[go: up one dir, main page]
More Web Proxy on the site http://driver.im/
You seem to have javascript disabled. Please note that many of the page functionalities won't work as expected without javascript enabled.
 
 
Sign in to use this feature.

Years

Between: -

Subjects

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Journals

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Article Types

Countries / Regions

remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline
remove_circle_outline

Search Results (982)

Search Parameters:
Keywords = H. pylori

Order results
Result details
Results per page
Select all
Export citation of selected articles as:
18 pages, 2245 KiB  
Article
Helicobacter pylori HP0135 Is a Small Lipoprotein That Has a Role in Outer Membrane Stability
by Doreen Nguyen, Rachel G. Ivester, Kyle Rosinke and Timothy R. Hoover
Molecules 2025, 30(2), 204; https://doi.org/10.3390/molecules30020204 - 7 Jan 2025
Viewed by 450
Abstract
Helicobacter pylori is a Gram-negative bacterium and human pathogen that is linked to various gastric diseases, including peptic ulcer disease, chronic gastritis, and gastric cancer. The filament of the H. pylori flagellum is surrounded by a membranous sheath that is contiguous with the [...] Read more.
Helicobacter pylori is a Gram-negative bacterium and human pathogen that is linked to various gastric diseases, including peptic ulcer disease, chronic gastritis, and gastric cancer. The filament of the H. pylori flagellum is surrounded by a membranous sheath that is contiguous with the outer membrane. Proteomic analysis of isolated sheathed flagella from H. pylori B128 identified the lipoprotein HP0135 as a potential component of the flagellar sheath. HP0135 is a small protein, with the mature HP0135 lipoprotein only 28 amino acid residues in length. Deletion of hp0135 in H. pylori B128 resulted in morphological abnormalities that included extensive formation of outer membrane vesicles and increased frequency of mini-cells. Introducing a plasmid-borne copy of hp0135 into the H. pylori Δhp0135 mutant suppressed the morphological abnormalities. The phenotype of the Δhp0135 mutant suggests HP0135 has roles in stabilizing the cell envelope and cell division. Full article
(This article belongs to the Section Macromolecular Chemistry)
Show Figures

Graphical abstract

Graphical abstract
Full article ">Figure 1
<p>Alignment of the amino acid sequences of HP0135 homologs and the predicted tertiary structure of HP0135. (<b>A</b>) Amino acid sequences of HP0135 homologs were aligned using the Clustal Omega (<a href="http://www.ebi.ac.uk/jdispatcher/msa/clustalo" target="_blank">www.ebi.ac.uk/jdispatcher/msa/clustalo</a> (accessed on 10 September 2024)) sequence analysis tool [<a href="#B38-molecules-30-00204" class="html-bibr">38</a>]. HP0135 homologs are from the following species: <span class="html-italic">Helicobacter acinonychis</span> (Hac), <span class="html-italic">H. pylori</span> (Hpy), <span class="html-italic">Helicobacter</span> sp. 219-2 (219-2), <span class="html-italic">Helicobacter cetorum</span> (Hce), <span class="html-italic">Helicobacter suis</span> (Hsu), <span class="html-italic">Helicobacter ailurogastricus</span> (Hai), <span class="html-italic">Helicobacter</span> sp. NHP19-012 (19-012), <span class="html-italic">Helicobacter</span> sp. NHP22-001 (22-001), <span class="html-italic">Helicobacter heilmannii</span> ASB1.4 (Hhe), <span class="html-italic">Helicobacter</span> sp. NHP21005 (21005), <span class="html-italic">Helicobacter</span> sp. NHP19-003 (19-003), <span class="html-italic">Helicobacter bizzozeronii</span> (Hbi), <span class="html-italic">Helicobacter mehlei</span> (Hme), <span class="html-italic">Helicobacter salmonis</span> (Hsa), <span class="html-italic">Helicobacter baculiformis</span> (Hba), <span class="html-italic">Helicobacter felis</span> (Hfe), <span class="html-italic">Helicobacter cynogastricus</span> (Hcy), <span class="html-italic">Helicobacter</span> sp. L8 (L8), <span class="html-italic">Helicobacter vulpis</span> (Hvu), <span class="html-italic">Helicobacter</span> sp. 13S00477-4 (77-4), <span class="html-italic">Helicobacter</span> sp. 12S02232-10 (32-10), and <span class="html-italic">Helicobacter</span> sp. 11S02596-1 (96-1). For each amino acid position, identical amino acids are indicated with an asterisk and similar amino acids are indicated with one dot. Hydrophobic, polar, basic, and acidic amino acid residues are indicated in red, green, magenta, and blue, respectively. The predicted signal peptide cleavage site is indicated by the red arrow. (<b>B</b>) Tertiary structure of HP0135 prolipoprotein predicted by AlphaFold2 [<a href="#B39-molecules-30-00204" class="html-bibr">39</a>]. Regions in blue indicate a high confidence for predicted structure, while regions in yellow indicate a lower confidence for predicted structure. The position of Cys-17, which is the site of cleavage, is indicated. The position of Ser-31, which is the last amino acid residue within a well-ordered tertiary structure, is also indicated.</p>
Full article ">Figure 2
<p>TEM images of wild-type <span class="html-italic">H. pylori</span> B128, the original Δ<span class="html-italic">hp0135</span> mutant, and the complemented Δ<span class="html-italic">hp0135</span> strain. (<b>A</b>) TEM field showing examples of <span class="html-italic">H. pylori</span> Δ<span class="html-italic">hp0135</span> mutant cells. The black arrows indicate cells in the field that have OMVs. The yellow arrow indicates a cell that appears to be undergoing lysis. (<b>B</b>) An example of a mini-cell formed by the <span class="html-italic">H. pylori</span> Δ<span class="html-italic">hp0135</span> mutant is indicated by the white arrow. The black arrow indicates a normal-length cell that displays OMVs at the cell pole. (<b>C</b>) TEM field showing wild-type <span class="html-italic">H. pylori</span> B128 cells. Polar flagella are indicated by the black arrows. (<b>D</b>) TEM field showing examples of cells of Δ<span class="html-italic">hp0135</span> mutant that was complemented with a plasmid-borne copy of <span class="html-italic">hp0135</span>. The arrow indicates a cell that has OMVs. (<b>E</b>) Proportion of cells with OMVs in Δ<span class="html-italic">hp0135</span> mutant, wild-type <span class="html-italic">H. pylori</span> B128, and Δ<span class="html-italic">hp0135</span>/pHP0135 strain. Cells were counted from two biological replicates for each strain, and the number of cells counted for the Δ<span class="html-italic">hp0135</span> mutant, wild type, and Δ<span class="html-italic">hp0135</span>/pHP0135 strain were 139, 78, and 60, respectively. The proportion of cells with OMVs in the Δ<span class="html-italic">hp0135</span> mutant was significantly higher compared to the wild type and the complemented strain as determined by Fisher’s exact test (<span class="html-italic">p</span>-value &lt; 0.00001).</p>
Full article ">Figure 3
<p>TEM images of strains RIH3A and RIH3C. (<b>A</b>,<b>B</b>) TEM images of strain RIH3A. The black arrows indicate flagellated cells. (<b>C</b>,<b>D</b>) TEM images of strain RIH3C. The black arrows indicate flagellated cells.</p>
Full article ">
14 pages, 2412 KiB  
Article
Gastric Microbiota Associated with Gastric Precancerous Lesions in Helicobacter pylori-Negative Patients
by Han-Na Kim, Min-Jeong Kim, Jonathan P. Jacobs and Hyo-Joon Yang
Microorganisms 2025, 13(1), 81; https://doi.org/10.3390/microorganisms13010081 - 3 Jan 2025
Viewed by 523
Abstract
Studies on the gastric microbiota associated with gastric precancerous lesions remain limited. This study aimed to profile the gastric mucosal microbiota in patients with Helicobacter pylori-negative precancerous lesions. Gastric mucosal samples were obtained from 67 H. pylori-negative patients, including those with [...] Read more.
Studies on the gastric microbiota associated with gastric precancerous lesions remain limited. This study aimed to profile the gastric mucosal microbiota in patients with Helicobacter pylori-negative precancerous lesions. Gastric mucosal samples were obtained from 67 H. pylori-negative patients, including those with chronic gastritis (CG), intestinal metaplasia (IM), and dysplasia. The V3–V4 region of the 16S rRNA gene was sequenced and analyzed. No significant difference was observed in the alpha or beta diversity of the gastric microbiota among the groups. However, a taxonomic analysis revealed a significant enrichment of Lautropia mirabilis and the depletion of Limosilactobacillus reuteri, Solobacxterium moorei, Haemophilus haemolyticus, and Duncaniella dubosii in the IM and dysplasia groups compared to those in the CG group. Prevotella jejuni and the genus Parvimonas were enriched in the IM group. A predictive functional analysis revealed enrichment of the ornithine degradation pathway in the IM and dysplasia groups, suggesting its role in persistent gastric mucosal inflammation associated with gastric precancerous lesions. The gastric microbiota associated with H. pylori-negative gastric precancerous lesions showed an increased abundance of oral microbes linked to gastric cancer and a reduction in anti-inflammatory bacteria. These alterations might contribute to chronic gastric mucosal inflammation, promoting carcinogenesis in the absence of H. pylori infection. Full article
(This article belongs to the Special Issue Correlations Between the Gastrointestinal Microbiome and Diseases)
Show Figures

Figure 1

Figure 1
<p>A flowchart of the study.</p>
Full article ">Figure 2
<p>Alpha diversity in the gastric microbiota did not significantly differ among the chronic gastritis (CG), intestinal metaplasia (IM), and dysplasia groups. (<b>a</b>) Observed amplicon sequence variants, (<b>b</b>) Pielou’s evenness, (<b>c</b>) Shannon index, and (<b>d</b>) Faith’s phylogenetic diversity. Horizontal lines indicate medians. No significant difference was found among the groups for any alpha diversity index after adjusting for age and sex.</p>
Full article ">Figure 3
<p>Overall gastric microbiota composition did not significantly differ between the chronic gastritis (CG), intestinal metaplasia (IM), and dysplasia groups in beta diversity analysis. (<b>a</b>) Bray–Curtis dissimilarity, (<b>b</b>) Jaccard distance, (<b>c</b>) unweighted UniFrac distance, and (<b>d</b>) weighted UniFrac distance. Visualization was performed using principal coordinate analysis. Effect size and significance were assessed using permutational multivariate analysis of variance with 10,000 permutations, adjusting for age and sex. Ellipses represent 95% of data points for each group.</p>
Full article ">Figure 4
<p>Gastric mucosal microbiota did not differ at the phylum level among the chronic gastritis (CG), intestinal metaplasia (IM), and dysplasia groups. Although a trend of decreasing relative abundance of Proteobacteria and increasing relative abundance of Firmicutes was observed from the CG to the IM and dysplasia groups, no statistically significant difference was observed among the groups by DESeq2 analysis after adjusting for age and sex.</p>
Full article ">Figure 5
<p>Differentially abundant taxa were identified in patients with gastric precancerous lesions compared to those without. Differentially abundant taxa are shown for (<b>a</b>) the comparison between intestinal metaplasia (IM) and chronic gastritis (CG) groups and (<b>b</b>) the comparison between dysplasia and CG groups, identified at the species level using DESeq2 analysis. The effect size represents log<sub>2</sub> fold changes between the groups with 95% confidence intervals. Dot size reflects normalized relative abundance, and colors indicate corresponding phyla. Statistical significance was determined as a false discovery rate <span class="html-italic">q</span>-value &lt; 0.1, with adjustment for age and sex.</p>
Full article ">
15 pages, 3233 KiB  
Article
Imaging the Ultrastructure of Isolated Peptidoglycan Sacculi from Rod-Shaped Helicobacter pylori J99 Cells by Atomic Force Microscopy
by Daniel Amiteye, Jandirk Sendker and Fabian Herrmann
Molecules 2025, 30(1), 155; https://doi.org/10.3390/molecules30010155 - 3 Jan 2025
Viewed by 471
Abstract
Peptidoglycan is the basic structural polymer of the bacterial cell wall and maintains the shape and integrity of single cells. Despite years of research conducted on peptidoglycan’s chemical composition, the microscopic elucidation of its nanoscopic architecture still needs to be addressed more thoroughly [...] Read more.
Peptidoglycan is the basic structural polymer of the bacterial cell wall and maintains the shape and integrity of single cells. Despite years of research conducted on peptidoglycan’s chemical composition, the microscopic elucidation of its nanoscopic architecture still needs to be addressed more thoroughly to advance knowledge on bacterial physiology. Apart from the model organism Escherichia coli, ultrastructural imaging data on the murein architecture of Gram-negative bacteria is mostly missing today. This study therefore intended to further our understanding of bacterial physiology by the isolation of peptidoglycan sacculi from the Gram-negative bacterium Helicobacter pylori J99 and the subsequent nanoscopic imaging of the murein network by Atomic Force Microscopy (AFM). With the ability to purify peptidoglycan sacculi from H. pylori J99 for AFM by a modified peptidoglycan isolation protocol, nanoscopic imaging of the murein network by intermittent-contact AFM in air and under liquid yielded ultrastructural insights into the H. pylori J99 cell wall architecture. High-resolution data acquisition on isolated peptidoglycan from H. pylori J99 by AFM under liquid was performed and revealed a molecular network similar to available data from E. coli. Subsequent enzymatic digestion of the isolated H. pylori J99 sacculi and analysis of the resulting fragments by +ESI-LCMS confirmed the presence of N-acetylglucosamine as an additional marker for successful peptidoglycan isolation. By comparison of the nanoscopic sacculus dimensions of H. pylori J99 to E. coli NU14, this study also identified specific differences in the sacculus morphology of both Gram-negative pathogenic bacteria. Full article
Show Figures

Figure 1

Figure 1
<p>Representative phase-contrast light microscopic image of a <span class="html-italic">H. pylori</span> J99 suspension culture at an OD<sub>600</sub> of 0.2. The predominant cell shape under typical high-passage in vitro cultivation conditions was a rod-like morphology.</p>
Full article ">Figure 2
<p>Representative AFM images of isolated, purified, and immobilized <span class="html-italic">H. Pylori</span> J99 (<b>A</b>–<b>D</b>) and <span class="html-italic">E. coli</span> NU14 (<b>E</b>) peptidoglycan sacculi recorded by intermittent-contact mode AFM under ambient conditions in air. Intermittent-contact mode AFM imaging in air yielded valuable ultrastructural insights into general <span class="html-italic">H. Pylori</span> J99 peptidoglycan sacculus morphology. The expected nanoscopic murein structure with typical septal morphology (exemplary septum marked with white arrow in (<b>A</b>)) and delicate bands with perpendicular orientation to the growth axis of single bacteria cells (blue arrow in (<b>D</b>)) were clearly recognized. Note the overall rather low number of intracellular remnants as a result of the modified isolation protocol employed for <span class="html-italic">H. Pylori</span> J99 sacculus purification (representative intracellular remnant marked by yellow arrow in (<b>C</b>)). A representative peptidoglycan sacculus from <span class="html-italic">E. coli</span> NU14 of this study is shown in (<b>E</b>).</p>
Full article ">Figure 3
<p>Representative morphological measurements on an isolated, purified, and immobilized <span class="html-italic">H. Pylori</span> J99 sacculus employing data collected by intermittent-contact mode AFM in air. Measurements are represented by typical section planes for each analyzed parameter (a and b). Dashed blue lines in a and b indicate reference points for the different measurements. Prior to any sectioning measurement, AFM images were flattened employing the 0th-order algorithm implemented in the software Nanoscope Analysis 3.0 (Bruker, Karlsruhe, Germany).</p>
Full article ">Figure 4
<p>Violin plots representing measurements of morphological characteristics from isolated murein sacculi of <span class="html-italic">H. pylori</span> J99 compared to corresponding measurements on <span class="html-italic">E. coli</span> NU14 sacculi prepared by the same isolation protocol (<b>A</b>–<b>C</b>). Altogether, nine isolated sacculi from both species were analyzed for each parameter (three sacculi for each of the three replicates per species). Each parameter was measured at least thrice for every sacculus. Statistical variance was analyzed employing the Student t-test algorithm implemented in the software GraphPad Prism 9 (n.s. = no significant difference, ** = <span class="html-italic">p</span> &lt; 0.01, **** = <span class="html-italic">p</span> &lt; 0.0001; GraphPad Prism 9, GraphPad Software, Boston, MA, USA). No significant differences were detected between the overall septum heights of <span class="html-italic">H. pylori</span> J99 and <span class="html-italic">E. coli</span> NU14 (<b>A</b>). Measurements of sacculus height (<b>B</b>) as well as sacculus roughness (<b>C</b>) data showed significant differences between the two Gram-negative species, indicating differing physiology of their peptidoglycan architecture and/or composition.</p>
Full article ">Figure 5
<p>Representative AFM height channel images of isolated <span class="html-italic">H. pylori</span> J99 peptidoglycan sacculi imaged by intermittent-contact mode AFM under liquid conditions. The modified isolation protocol of this study reproducibly enabled lower nm resolution on isolated sacculi from <span class="html-italic">H. pylori</span> J99, although true molecular resolution on single peptidoglycan strands was not reached. Nanoscopic insights into the peptidoglycan architecture of <span class="html-italic">H. pylori</span> J99 were established by AFM imaging in TRIS/HCl buffer. Representative image of two complete sacculi is shown in (<b>A</b>), details in images (<b>B</b>–<b>D</b>). Note the evenly distributed peptidoglycan network consisting of crosslinked macromolecules ((<b>B</b>–<b>D</b>), single strand-like macromolecule indicated with blue arrow in (<b>D</b>)). Additionally, typical dense and less dense regions of peptidoglycan architecture were recognized in the AFM data, attributable to the highly dynamic ultrastructure of peptidoglycan (more dense area highlighted in (<b>B</b>), less dense area highlighted in (<b>D</b>)).</p>
Full article ">Figure 6
<p>+ESI-LCMS of digested muropeptide of <span class="html-italic">Helicobacter pylori</span> J99. (<b>A</b>): Overview base peak chromatogram, full mass range (<span class="html-italic">m/z</span> 50–1500). (<b>B</b>): Extracted ion chromatogram indicative of the presence of the <span class="html-italic">N</span>-acetylglucosamine fragment at <span class="html-italic">m/z</span> 204.0866 [C<sub>8</sub>H<sub>13</sub>NO<sub>5</sub> + H]<sup>+</sup>. (<b>C</b>): +ESI-MS spectrum of the peak at 15 min. The theoretical ion mass of the protonated <span class="html-italic">N</span>-acteylglucosamine-fragment [C<sub>8</sub>H<sub>14</sub>NO<sub>5</sub>]<sup>+</sup> deviates from the measured ion mass of 204.0899 u by 3.2 mu, mΣ is 9.4.</p>
Full article ">
17 pages, 3257 KiB  
Article
Unveiling the Potency of Gardenia Extract Against H. pylori: Insights from In Vitro and In Vivo Studies
by Pornpen Werawatganone, Duangporn Werawatganon, Nattida Noonak, Maneerat Chayanupatkul, Tanittha Chatsuwan, Naruemon Klaikeaw, Walaisiri Muangsiri and Prasong Siriviriyakul
Biomedicines 2025, 13(1), 92; https://doi.org/10.3390/biomedicines13010092 - 2 Jan 2025
Viewed by 414
Abstract
Background and aim: Gardenia jasminoides (G. jasminoides) could treat various inflammatory diseases. This study aimed to investigate the effects of G. jasminoides fruit extract on gastric inflammation and protective mechanisms in Helicobacter pylori (H. pylori)-induced gastritis. Experimental procedure: G. [...] Read more.
Background and aim: Gardenia jasminoides (G. jasminoides) could treat various inflammatory diseases. This study aimed to investigate the effects of G. jasminoides fruit extract on gastric inflammation and protective mechanisms in Helicobacter pylori (H. pylori)-induced gastritis. Experimental procedure: G. jasminoides fruit extract was prepared and analyzed for geniposide content. The inhibitory effect of the extract on H. pylori growth was investigated using the disk diffusion method. The in vitro anti-inflammatory property of the extract was evaluated using the erythrocyte membrane stabilization method. Thirty-five male Sprague–Dawley rats were inoculated with H. pylori (108–1010 colony-forming unit/mL) and divided into five groups. Each group was treated with various doses of the extract (98–395 mg/kg). The serum and stomach tissue of the rats were evaluated using enzyme-linked immunosorbent assay, histopathology, and immunohistochemistry. Results and conclusions: The geniposide content in the dried extract was 8.12% ± 0.79% by dry weight. The inhibition zone was observed at the extract ≥ 1.97 mg/disk, and the extract presented anti-inflammatory potential. The H. pylori-inoculated rats had a significant increase in serum interleukin (IL)-17, IL-33, and gastric epidermal growth factor (EGF) levels and a significant decrease in serum prostaglandin E2 level (p < 0.05) in conjunction with the development of gastric inflammation on histopathology. The treatment of the extract could significantly decrease the serum IL-17, IL-33, and gastric EGF levels, significantly increase the serum PGE2 level (p < 0.05), and improve gastric histopathology. Thus, G. jasminoides fruit extract attenuated H. pylori-induced gastritis by inhibiting bacterial growth, reducing inflammation, and enhancing protective mechanisms. Full article
(This article belongs to the Special Issue Feature Reviews in Cell Death)
Show Figures

Figure 1

Figure 1
<p>Correlation of hemolysis inhibition and concentration of tested substances using heat-induced hemolysis (n = 3); (<b>A</b>) <span class="html-italic">G. jasminoides</span> extract, (<b>B</b>) diclofenac, standard geniposide, and calculated geniposide in the extract.</p>
Full article ">Figure 2
<p>The histopathological examination of gastric inflammation in all groups; (<b>A</b>) Control group, (<b>B</b>) Hp group, (<b>C</b>) Hp + gen8 group, (<b>D</b>) Hp + gen16 group, (<b>E</b>) Hp + gen32 group, black arrows indicating inflammatory cell infiltration, GE = gastric epithelium, LP = lamina propria, MM = muscularis mucosae (H&amp;E stain, 100× magnification, scale bar 90 µm).</p>
Full article ">Figure 3
<p>Histopathological examination of <span class="html-italic">H. pylori</span> colonization in Hp group; black arrows indicating <span class="html-italic">H. pylori</span> colonization. GE = gastric epithelium (Giemsa stain, 400× magnification, scale bar 20 µm).</p>
Full article ">Figure 4
<p>Effects of <span class="html-italic">H. pylori</span> and <span class="html-italic">G. jasminoides</span> extract on serum inflammatory cytokine levels in all groups; (<b>A</b>) serum IL-17 level, (<b>B</b>) serum IL-33 level (<sup>a</sup> <span class="html-italic">p</span> &lt; 0.05 vs. Control group, <sup>b</sup> <span class="html-italic">p</span> &lt; 0.05 vs. Hp group).</p>
Full article ">Figure 5
<p>Effects of <span class="html-italic">H. pylori</span> and <span class="html-italic">G. jasminoides</span> extract on serum PGE<sub>2</sub> in all groups (<sup>a.</sup><span class="html-italic">p</span> &lt; 0.05 vs. Control group; <sup>b</sup> <span class="html-italic">p</span> &lt; 0.05 vs. Hp group.</p>
Full article ">Figure 6
<p>Immunohistochemistry of EGF expression; (<b>A</b>) Control group, (<b>B</b>) <span class="html-italic">H. pylori</span> group, (<b>C</b>) Hp + gen8 group, (<b>D</b>) Hp + gen16 group, (<b>E</b>) Hp + gen32 group, (40× magnification)<tt>, </tt>and (<b>F</b>) <span class="html-italic">H. pylori</span> group with 400× magnification, yellow arrows indicating EGF expression.</p>
Full article ">Figure 7
<p>Effects of <span class="html-italic">H. pylori</span> and <span class="html-italic">G.jasminoides</span> extract on gastric EGF in all groups (<sup>a</sup> <span class="html-italic">p</span> &lt; 0.05 vs. Control group, <sup>b</sup> <span class="html-italic">p</span> &lt; 0.05 vs. Hp group).</p>
Full article ">
20 pages, 9893 KiB  
Review
The Influence of Gastric Microbiota and Probiotics in Helicobacter pylori Infection and Associated Diseases
by Jagriti Verma, Md Tanveer Anwar, Bodo Linz, Steffen Backert and Suneesh Kumar Pachathundikandi
Biomedicines 2025, 13(1), 61; https://doi.org/10.3390/biomedicines13010061 - 30 Dec 2024
Viewed by 484
Abstract
The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which [...] Read more.
The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which is equivalent to almost ten times the total number of cells of the human host. Helicobacter pylori is a known pathogen that colonizes the gastric mucosa of almost half of the world population. H. pylori is associated with several gastric diseases, including gastric cancer (GC) development. However, the impact of the gastric microbiota in the colonization, chronic infection, and pathogenesis is still not fully understood. Several studies have documented qualitative and quantitative changes in the microbiota’s composition in the presence or absence of this pathogen. Among the diverse microflora in the stomach, the Firmicutes represent the most notable. Bacteria such as Prevotella sp., Clostridium sp., Lactobacillus sp., and Veillonella sp. were frequently found in the healthy human stomach. In contrast, H.pylori is very dominant during chronic gastritis, increasing the proportion of Proteobacteria in the total microbiota to almost 80%, with decreasing relative proportions of Firmicutes. Likewise, H. pylori and Streptococcus are the most abundant bacteria during peptic ulcer disease. While the development of H. pylori-associated intestinal metaplasia is accompanied by an increase in Bacteroides, the stomachs of GC patients are dominated by Firmicutes such as Lactobacillus and Veillonella, constituting up to 40% of the total microbiota, and by Bacteroidetes such as Prevotella, whereas the numbers of H. pylori are decreasing. This review focuses on some of the consequences of changes in the gastric microbiota and the function of probiotics to modulate H. pylori infection and dysbiosis in general. Full article
(This article belongs to the Special Issue Inflammatory Chaos in Helicobacter pylori Infection)
Show Figures

Figure 1

Figure 1
<p>Changes in the gastric microbiota following <span class="html-italic">Helicobacter pylori</span> infection. Schematic representation of the predominant phyla of the gastric microbiota in <span class="html-italic">H. pylori</span>-negative (Hp-neg.) and in <span class="html-italic">H. pylori</span>-positive individuals (Hp-pos.) and in individuals with intestinal metaplasia (IM) or with GC.</p>
Full article ">Figure 2
<p><span class="html-italic">Helicobacter pylori</span> infection promoting and inhibiting major microbiota groups in pathogenesis. The dynamics of microbiota composition during <span class="html-italic">H. pylori</span> infection might be involved in the associated pathologies. <span class="html-italic">H. pylori</span> is a critical factor affecting the microbiota diversity in the gastric mucosa. In the context of an <span class="html-italic">H. pylori</span> infection, gastric microbiota groups can be inhibited or promoted. As per the available evidence, these two microbiota groups are functionally different in supporting or preventing the growth of <span class="html-italic">H. pylori</span>, immune responses, and pathogenesis of the associated diseases. Thus, the survival and successful colonization of <span class="html-italic">H. pylori</span> leads to dysbiosis, which favors persistence of infection.</p>
Full article ">
11 pages, 2522 KiB  
Article
Ultrasound Features of Helicobacter pylori-Related Gastritis
by Fulvia Terracciano, Antonella Marra, Veronica Nassisi, Chiara Lillo, Fabrizio Bossa, Sonia Carparelli, Francesco Cocomazzi, Maria Rosa Valvano, Giuseppe Losurdo, Alfredo Di Leo and Francesco Perri
Antibiotics 2025, 14(1), 12; https://doi.org/10.3390/antibiotics14010012 - 28 Dec 2024
Viewed by 428
Abstract
Background Abdominal ultrasound (US) is a reliable method for visualizing gastric wall layers and measuring their thickness. The objective of this study is to characterize the ultrasound features of H. pylori-induced gastritis and assess its predictive potential role for this condition. Methods [...] Read more.
Background Abdominal ultrasound (US) is a reliable method for visualizing gastric wall layers and measuring their thickness. The objective of this study is to characterize the ultrasound features of H. pylori-induced gastritis and assess its predictive potential role for this condition. Methods A cohort of 119 patients underwent gastroscopy with biopsy and abdominal US to evaluate antral wall thickness (AWT), submucosal wall thickness (SLT), mucosal wall thickness (MLT), gastric motility, and the presence of ingested material. They were divided into three groups: group A (normal mucosa without H. pylori infection), group B (gastritis H. pylori negative) and group C (gastritis H. pylori positive). Results: SLT and reduced gastric motility were significantly increased in the H. pylori gastritis group (p < 0.001). Multivariate analysis identified SLT as the only significant independent predictor of H. pylori gastritis (p < 0.001). An SLT threshold of 1.55 mm was determined as optimal for differentiating H. pylori-positive patients from -negative, yielding a sensitivity of 77% and a specificity of 72%. Conclusions These findings suggest that H. pylori gastritis is characterized by submucosal layer thickening and impaired gastric motility. Full article
(This article belongs to the Section Antibiotic Therapy in Infectious Diseases)
Show Figures

Figure 1

Figure 1
<p>Stomach explored by convex probe containing food ingests in <span class="html-italic">Helicobacter pylori</span>-positive patient. The red arrow in the image indicates the presence of ingested material in the stomach.</p>
Full article ">Figure 2
<p>Transversal section of gastric antrum with different layers of the wall. The red line represents the anterior wall of the antrum, showing the normal alternation of layers. Starting from inside: lumen–mucosa interface, mucosa, submucosa, muscularis, and serosa. (<b>a</b>) Antrum in a patient without Hp-related gastritis, with a normal submucosal layer. (<b>b</b>) Antrum in a patient with Hp-related gastritis, showing a thickened submucosa, marked by a red arrow.</p>
Full article ">Figure 3
<p>ROC curve between group 1 (green line) and group 2 (blue line).</p>
Full article ">Figure 4
<p>Schematic representation of the alternation of the layers of the gastric wall.</p>
Full article ">
12 pages, 1170 KiB  
Article
Discovery of Isograndidentatin D, a Novel Phenolic Glycoside, and Anti-Helicobacter pylori Phenolics from Salix koreensis Twigs
by Yoon Seo Jang, Dong-Min Kang, Yoon-Joo Ko, Moon-Jin Ra, Sang-Mi Jung, Mi-Jeong Ahn, Seulah Lee and Ki Hyun Kim
Plants 2024, 13(24), 3603; https://doi.org/10.3390/plants13243603 - 23 Dec 2024
Viewed by 349
Abstract
Salix koreensis Anderss (Salicaceae), commonly referred to as Korean willow, is native to East Asia, particularly Korea and China, and it has been used in traditional Korean folk medicine for its potent anti-inflammatory, analgesic, and antioxidant properties. In our ongoing research efforts to [...] Read more.
Salix koreensis Anderss (Salicaceae), commonly referred to as Korean willow, is native to East Asia, particularly Korea and China, and it has been used in traditional Korean folk medicine for its potent anti-inflammatory, analgesic, and antioxidant properties. In our ongoing research efforts to discover biologically new natural products, phytochemical analysis on an ethanolic extract of S. koreensis twigs yielded the isolation and identification of ten phenolic compounds (110), including a newly discovered phenolic glycoside (1) named isograndidentatin D, isolated via HPLC purification. The structure of compound 1 was determined through extensive 1D and 2D NMR spectral data analysis and high-resolution electrospray ionization mass spectrometry (HR-ESIMS). Its absolute configuration was established using DP4+ probability analysis combined with gauge-including atomic orbital NMR chemical shift calculations and chemical reaction methods. The other known compounds were identified as isograndidentatin B (2), trichocarposide (3), glanduloidin C (4), tremuloidin (5), 3-O-acetylsalicin (6), 2-O-acetylsalicin (7), salicin (8), salireposide (9), and coumaric acid (10), confirmed by comparing their NMR spectra with previously reported data and further verified through liquid chromatography/mass spectrometry (LC/MS) analysis. The isolated compounds 110 were tested for their anti-Helicobacter pylori activities. Among these, compounds 4 and 5 demonstrated moderate anti-H. pylori activity at a concentration of 100 μM. Specifically, compound 5 showed an inhibitory activity of 35.9 ± 5.4%, making it slightly more potent than compound 4, with 34.0 ± 1.0% inhibition. These results were comparable to that of quercetin, a known anti-H. pylori agent used as a positive control in this study, which showed 38.4 ± 2.3% inhibition. The remaining compounds exhibited very weak inhibitory effects. This study highlights the potential of S. koreensis twigs as a valuable natural source of bioactive compounds for therapeutic applications against H. pylori. Full article
Show Figures

Figure 1

Figure 1
<p>Chemical structures of compounds <b>1</b>–<b>10</b>.</p>
Full article ">Figure 2
<p>Key <sup>1</sup>H-<sup>1</sup>H COSY (<span class="html-fig-inline" id="plants-13-03603-i001"><img alt="Plants 13 03603 i001" src="/plants/plants-13-03603/article_deploy/html/images/plants-13-03603-i001.png"/></span>) and HMBC (<span class="html-fig-inline" id="plants-13-03603-i002"><img alt="Plants 13 03603 i002" src="/plants/plants-13-03603/article_deploy/html/images/plants-13-03603-i002.png"/></span>) correlations for compound <b>1</b>.</p>
Full article ">Figure 3
<p>DP4+ analysis and probability scores for compound <b>1</b> with <b>1a</b>/<b>1b</b>.</p>
Full article ">
11 pages, 328 KiB  
Article
Association Between Chlamydia trachomatis and Helicobacter pylori with Inflammation in Polycystic Ovary Syndrome: A Cross-Sectional Study
by Yeşim Alpay Çağlar and Mine Islimye Taşkin
Medicina 2024, 60(12), 2102; https://doi.org/10.3390/medicina60122102 - 22 Dec 2024
Viewed by 419
Abstract
Objective: Chronic low-grade inflammation occurs in polycystic ovary syndrome (PCOS), and there are many contributing factors. In this study, we aimed to investigate Helicobacter pylori and Chlamydia trachomatis infections in patients with PCOS and to evaluate the association between these microorganisms and [...] Read more.
Objective: Chronic low-grade inflammation occurs in polycystic ovary syndrome (PCOS), and there are many contributing factors. In this study, we aimed to investigate Helicobacter pylori and Chlamydia trachomatis infections in patients with PCOS and to evaluate the association between these microorganisms and the inflammatory process in the etiology of the disease. Materials and Methods: This comparative cross-sectional clinical study was conducted at Balıkesir University Hospital and included 40 female patients diagnosed with PCOS in the gynecology outpatients clinic and 40 healthy female controls. Demographic data were recorded. Blood hormone profiles and biochemical parameters were analyzed. An enzyme-linked immunosorbent assay test kit was used to measure H. pylori IgG and C. trachomatis IgG. Results: According to the analysis of the study data, there was no significant association between the PCOS and non-PCOS groups with regard to the presence of Helicobacter pylori IgG (p = 0.1) and Chlamydia trachomatis IgG (p = 0.338). CRP levels were significantly higher in the PCOS group (p = 0.001). In the subgroup analyses, the CRP levels were not significantly different between the H. pylori and C. trachomatis antibody-positive and -negative groups. Diabetes mellitus was significantly associated with PCOS (p = 0.005). The smoking rate was significantly higher in the control group than in the PCOS group (p = 0.036). Compared to the control group, the BMI, LH, HOMA-IR, TSH, and TG levels were significantly higher in participants with PCOS (p = 0.000; p = 0.004; p = 0.001; p = 0.001; p = 0.043; p = 0.000). FSH was lower in PCOS patients compared to controls (p = 001). In the subgroup analyses, no significant differences were found between the H. pylori and C. trachomatis antibody-positive and -negative groups. Conclusions: PCOS is characterized by chronic nonspecific low-grade inflammation. The etiopathogenesis of PCOS involves comorbidities that cause a chronic inflammatory process. However, the possible infective causes still seem to be open to investigation. In particular, studies on microbiota and periodontal diseases in PCOS may provide important contributions. Full article
(This article belongs to the Section Infectious Disease)
23 pages, 4328 KiB  
Article
Herbal Extracts Mixed with Essential Oils: A Network Approach for Gastric and Intestinal Motility Disorders
by Roberta Budriesi, Ivan Corazza, Simone Roncioni, Roberta Scanferlato, Dalila De Luca, Carla Marzetti, Roberto Gotti, Nicola Rizzardi, Christian Bergamini, Matteo Micucci, Davide Roncarati and Laura Beatrice Mattioli
Nutrients 2024, 16(24), 4357; https://doi.org/10.3390/nu16244357 - 17 Dec 2024
Viewed by 674
Abstract
Background: Three herbal extracts (Asparagus racemosus Willd., Tabebuia avellanedae Lorentz, and Glycyrrhiza glabra L.) were mixed with three essential oils (Foeniculum vulgare Mill., Mentha piperita L., and Pimpinella anisum L.) to formulate a product (HEMEO) whose active compounds include saponins and [...] Read more.
Background: Three herbal extracts (Asparagus racemosus Willd., Tabebuia avellanedae Lorentz, and Glycyrrhiza glabra L.) were mixed with three essential oils (Foeniculum vulgare Mill., Mentha piperita L., and Pimpinella anisum L.) to formulate a product (HEMEO) whose active compounds include saponins and steroids in Asparagus racemosus, known for their anti-inflammatory properties; glycyrrhizin and flavonoids in Glycyrrhiza glabra, which exhibit gastroprotective and antispasmodic effects; menthol in Mentha piperita, contributing with antispasmodic and antimicrobial properties; and anethole and polyphenols in Pimpinella anisum, which modulate intestinal motility and offer antimicrobial activity. Objective: HEMEO was formulated for applications in intestinal motility disorders. Methods: HEMEO was evaluated for spontaneous and induced motility effects in isolated guinea pig ileum, colon, and stomach. Ex vivo experiments were conducted using LabChart software v7.0, and the product’s antibacterial action against Helicobacter pylori and its antioxidant effects were assessed through disc diffusion and FRAP assays. The presence of the volatile compounds in the formulation was confirmed by GC-MS analysis; the TPC of HEMEO, determined using the Folin–Ciocalteu method, was 9.925 ± 0.42 mg GAE/g. Conclusions: HEMEO showed a phenolic content correlated with its antioxidant potential and in addition inhibited H. pylori growth and demonstrated notable antioxidant properties, suggesting its role as a supportive agent in digestive processes and in managing motility disorders. Full article
Show Figures

Figure 1

Figure 1
<p>Overview of experimental design of HEMEO.</p>
Full article ">Figure 2
<p>Plants pictures and chemical structure of key compounds found in the plant extracts and essential oils.</p>
Full article ">Figure 3
<p>Example of experimental original recording of the concentration–response curve of HEMEO on spontaneous longitudinal (Long) stomach basal contractility. (<b>a</b>) Spontaneous contraction (SC) signals for each concentration; (<b>b</b>) mean contraction amplitude (MCA) and spontaneous contraction variability (SCV), represented as error bars in the MCA plot and contraction percentage variation for the control (BSMA) for each considered condition; all the comparisons resulted in being statistically significant (<span class="html-italic">p</span> &lt; 0.05); (<b>c</b>) power spectral density (PSD) and percentage variations. Despite statistically significant differences between muscular tones at different HEMEO concentrations, the MCA variations are not physiologically significant (less than 20%). MF and HF bands values increase over 50% only for concentrations of 5.0 mg/mL and 10 mg/mL, suggesting a slight increase in mixing and pain.</p>
Full article ">Figure 4
<p>Example of experimental original recording of the concentration–response curve of HEMEO on spontaneous longitudinal (Long) ileum basal contractility. (<b>a</b>) Spontaneous contraction (SC) signals for each concentration; (<b>b</b>) mean contraction amplitude (MCA) and spontaneous contraction variability (SCV), represented as error bars in the MCA plot and contraction percentage variation for the control (BSMA) for each considered condition; not statistically significant differences (<span class="html-italic">p</span> &gt; 0.05) between MCAs at different concentrations are reported in the graph with a curly bracket. All the comparisons not reported are to be considered significant (<span class="html-italic">p</span> &lt; 0.05); (<b>c</b>) power spectral density (PSD) and percentage variations. Longitudinal tones present a biphasic behavior: it increases for 0.1 mg/mL concentrations and then decreases until a maximum difference of −60%. LF and HF present the same tend.</p>
Full article ">Figure 5
<p>Example of experimental original recording of the concentration–response curve of HEMEO on spontaneous longitudinal (Long) colon basal contractility. (<b>a</b>) Spontaneous contraction (SC) signals for each concentration; (<b>b</b>) mean contraction amplitude (MCA) and spontaneous contraction variability (SCV), represented as error bars in the MCA plot and contraction percentage variation for the control (BSMA) for each considered condition; all the comparisons reported resulted statistically significant (<span class="html-italic">p</span> &lt; 0.05); (<b>c</b>) power spectral density (PSD) and percentage variations. Longitudinal tones present a biphasic behavior: it increases for 0.1 mg/mL concentrations and then decreases until a maximum difference of −80%. LF and HF bands present the same biphasic trend. MF has a maximum increase of 300% at 0.5 mg/mL, then decreases after 5.0 mg/mL.</p>
Full article ">Figure 6
<p>Effect of HEMEO on histamine-induced contraction in isolated guinea pig ileum (<b>a</b>) and in spontaneously beating right atrium (<b>b</b>). Cumulative concentration–response curves were obtained before and after exposure to HEMEO (1 mg/mL) for 30 min. Each point is the mean ± SEM (<span class="html-italic">n</span> = 5–6). Where error bars are not shown, these are covered by the point itself.</p>
Full article ">Figure 7
<p>(<b>a</b>) The antioxidant power of the HEMEO solution was measured using the FRAP assay. (<b>b</b>) Comparison of 1 mg/mL HEMEO antioxidant power with the reference compound ascorbate.</p>
Full article ">Figure 8
<p>Schematic diagram showing the detail of the experimental design.</p>
Full article ">
11 pages, 3755 KiB  
Article
Experience of Metronidazole Triple Therapy After Clarithromycin Triple Therapy Failure for Helicobacter pylori Eradication in Korea
by Chang-Min Lee, Seong-Je Kim, Jung-Woo Choi, Hyun-Chin Cho and Ok-Jae Lee
J. Clin. Med. 2024, 13(24), 7658; https://doi.org/10.3390/jcm13247658 - 16 Dec 2024
Viewed by 406
Abstract
Background/Objectives: Bismuth quadruple therapy (BQT) is recommended as the best second-line regimen after failure of first-line clarithromycin triple therapy (CTT) for Helicobacter pylori eradication. However, there are some limitations to this approach, including the lack of an appropriate sequel regimen after failure of [...] Read more.
Background/Objectives: Bismuth quadruple therapy (BQT) is recommended as the best second-line regimen after failure of first-line clarithromycin triple therapy (CTT) for Helicobacter pylori eradication. However, there are some limitations to this approach, including the lack of an appropriate sequel regimen after failure of BQT and complicated administration. Metronidazole triple therapy (MTT) is simple to administer, but it is not widely recommended. This study was conducted to determine the efficacy of MTT as second-line regimen for H. pylori eradication after failure of CTT. Methods: We retrospectively reviewed the medical records of the Korean patients with H. pylori infection who underwent second-line treatment after failure of first-line CTT from October 2013 to October 2019. The efficacy of MTT and BQT for H. pylori eradication was compared. Results: The eradication rate in the BQT group tended to be higher than that in the MTT group; however, the difference was not statistically significant (208/233, 89.3% versus 244/284, 85.9%, p = 0.287). Among 40 patients with second-line MTT eradication failure, 21 received the third-line BQT, and 15 showed successful eradication (15/21, 71.4%). In the men 70 years or older, the eradication rate of MTT was lower than that of BQT without statistical significance (75.8% versus 94.1%, p = 0.141). Conclusions: These findings suggested that MTT could be a second-line treatment option, reserving BQT for Helicobacter pylori eradication after first line CTT failure, except in elderly men 70 years or older. Full article
Show Figures

Figure 1

Figure 1
<p>Flow chart of enrollment. Metronidazole triple therapy, MTT; bismuth quadruple therapy, BQT; quinolone triple therapy, QTT.</p>
Full article ">Figure 2
<p>Comparison of second-line eradication rates for <span class="html-italic">Helicobacter pylori</span> between metronidazole triple therapy (MTT) and bismuth quadruple therapy (BQT) groups according to age and sex. MTT, metronidazole triple therapy; BQT, bismuth quadruple therapy.</p>
Full article ">Figure 3
<p>Proportion of the regimens that ultimately succeeded in eradication of <span class="html-italic">Helicobacter pylori</span> infection in the metronidazole triple therapy (MTT) and bismuth quadruple therapy (BQT) groups. MTT, metronidazole triple therapy; BQT, bismuth quadruple therapy; QTT, quinolone triple therapy (quinolone, amoxicillin, proton pump inhibitor). In the graph, the wavy midline break indicates omitted value for clarity.</p>
Full article ">
12 pages, 2699 KiB  
Article
Pathological In Vivo Analysis of Helicobacter DNA Infection in Stomach Cells Using Carbon Nanotube Microsensor
by Kyung Lee, Sihyun Jun, Yeseul Oh, Seojun Lee, Ye Jun Oh, Keum Sook Kim and Suw Young Ly
Microorganisms 2024, 12(12), 2531; https://doi.org/10.3390/microorganisms12122531 - 8 Dec 2024
Viewed by 874
Abstract
The WHO has classified Helicobacter pylori as a group 1 carcinogen for stomach cancer since early 1994. However, despite the high prevalence of Helicobacter pylori infection, only about 3% of infected people eventually develop gastric cancer.Biomolecular detections of Helicobacter pylori(HP) were compared using [...] Read more.
The WHO has classified Helicobacter pylori as a group 1 carcinogen for stomach cancer since early 1994. However, despite the high prevalence of Helicobacter pylori infection, only about 3% of infected people eventually develop gastric cancer.Biomolecular detections of Helicobacter pylori(HP) were compared using specially modified sensors and fluorine immobilized on a carbon nanotube (HFCNT) electrode, which yielded sensitive results. Handheld voltammetric circuits were used for optimization. An anodic voltammogram of HP molecular oxidation was obtained at 0.0 V ± 0.1 (versus the Ag/AgCl/KCl) in a 0.1 ± 0.2 M NH4H2PO4 electrolyte solution. Under optimized conditions, the analytical working range was 2.98 × 103–22.127 × 10−3 CFU/mL HP using square wave (SW) stripping voltammetry, precision of R2 = 0.9857 ± 0.0005 (SWSV), the detection limit approached to 2.5 × 102 CFU/mL HP (S/N = 3).The developed techniques have been applied to diagnosis of early-stage HP infections using stomach tissue from healthy humans and gastric patients. Full article
Show Figures

Figure 1

Figure 1
<p>(<b>A</b>) Comparisons of the PE, HFCNT, HGCNT, and DNACNT in 0.03, 0.06, and 0.09 mL (2.98 × 10<sup>3</sup> CFU/mL) HP concentrations using optimum SW anodic conditions with optimum parameters. (<b>B</b>) Cyclic voltammetry from 0.003 to 0.024 mL HP concentration via HFPE in a 0.1 M ammonium phosphate solution (pH 4.5) with optimum parameters, and theDNA sequence (5′-ATGGAAATACAACAAACACAC-3′ and 3′-CTGCTTGAATGCGCCAAAC-5′ for vacAs1/s2 while for vacAm1 and vacAm2 the primers were 5′-GTCAAAATGCGGTCATGG-3′ and 3′-CCATTGGTACCTGTAGAAAC-5′ and 5GGAGCCCCAGGAAACATTG-3′ and 3′-CATAACTAGCGCCTTGCAC-5′, respectively). (<b>C</b>) FE-SEM scanning of the cultivated HP cells showing a 10.0 kV accelerated voltage with 10,000 times magnification of a secondary electron image and width of 8.1 mm.</p>
Full article ">Figure 2
<p>(<b>A</b>) SWSV accumulation time variations from 15 to 200 s and incremental potential variations from 5 to 40 mV with a 0.01 mL HP concentration in a 4.6-pH 0.1 M NH<sub>4</sub>H<sub>2</sub>PO<sub>4</sub> electrolyte solution. (<b>B</b>) Electrode stability in the (<b>A</b>) solution for 15 repetitions with the optimum SW conditions in <a href="#microorganisms-12-02531-f003" class="html-fig">Figure 3</a>A.</p>
Full article ">Figure 3
<p>(<b>A</b>) SWSV anodic 0.003–0.08 mL HP (5.613 × 10<sup>−3</sup>–3.92 × 10<sup>−4</sup> CFU/mL HP) added to a 0.1 M NH<sub>4</sub>H<sub>2</sub>PO<sub>4</sub> solution. SW stripping: 50 mV amplitude, 20 Hz frequency, −1.0 V accumulation potential, and 200s accumulation time were used with a pH of 4.75. (<b>B</b>) Addition of 1–9 mL of diluted stomach tissue from healthy patients via SWSV. (<b>C</b>) Simulated illustration being applied, shows real time diagnosis of Helicobacter pylori virus living in the stomach, skin-coated tattoo sensor and diagnostic circuit, pain transmission neurodiagnostic network, and 3-electrode systems of amplified operational voltammetricnetwork.(<b>D</b>): Food fish. Real-time diagnostic experiment with in vivo sensor insertion.</p>
Full article ">Figure 3 Cont.
<p>(<b>A</b>) SWSV anodic 0.003–0.08 mL HP (5.613 × 10<sup>−3</sup>–3.92 × 10<sup>−4</sup> CFU/mL HP) added to a 0.1 M NH<sub>4</sub>H<sub>2</sub>PO<sub>4</sub> solution. SW stripping: 50 mV amplitude, 20 Hz frequency, −1.0 V accumulation potential, and 200s accumulation time were used with a pH of 4.75. (<b>B</b>) Addition of 1–9 mL of diluted stomach tissue from healthy patients via SWSV. (<b>C</b>) Simulated illustration being applied, shows real time diagnosis of Helicobacter pylori virus living in the stomach, skin-coated tattoo sensor and diagnostic circuit, pain transmission neurodiagnostic network, and 3-electrode systems of amplified operational voltammetricnetwork.(<b>D</b>): Food fish. Real-time diagnostic experiment with in vivo sensor insertion.</p>
Full article ">
29 pages, 14685 KiB  
Article
Helicobacter pylori Inhibition, Gastritis Attenuation, and Gut Microbiota Protection in C57BL/6 Mice by Ligilactobacillus salivarius NCUH062003
by Junyi Li, Xiaoyan Xu, Shiyu Yang, Kui Liu, Min Wu, Mingyong Xie and Tao Xiong
Microorganisms 2024, 12(12), 2521; https://doi.org/10.3390/microorganisms12122521 - 7 Dec 2024
Viewed by 852
Abstract
Helicobacter pylori (H. pylori), one of the most prevalent pathogenic bacteria worldwide, is the leading cause of gastritis, gastric intestinal metaplasia, and gastric cancer. Antibiotics, the conventional treatment for eliminating H. pylori, often lead to severe bacterial resistance, gut dysbiosis, [...] Read more.
Helicobacter pylori (H. pylori), one of the most prevalent pathogenic bacteria worldwide, is the leading cause of gastritis, gastric intestinal metaplasia, and gastric cancer. Antibiotics, the conventional treatment for eliminating H. pylori, often lead to severe bacterial resistance, gut dysbiosis, and hepatic insufficiency and fail to address the inflammatory response or gastric mucosal damage caused by H. pylori infection. In this study, based on 10-week animal experiments, two models of L. salivarius NCUH062003 for the prophylaxis and therapy of H. pylori infection in C57BL/6 mice were established; a comprehensive comparative analysis was performed to investigate the anti-H. pylori effect of probiotics, the reduction in inflammation, and repair of gastric mucosal damage. ELISA, immunohistochemistry, and pathology analyses showed that NCUH062003 decreased the expression of pro-inflammatory cytokine interleukins (IL-1β, IL-6) and myeloperoxidase (MPO) and reduced neutrophil infiltration in the gastric mucosa lamina propria. Immunofluorescence and biochemical analysis showed that NCUH062003 resisted gastric epithelial cell apoptosis, increased the level of superoxide dismutase (SOD) in gastric mucosa, and promoted the expression of tight junction protein ZO1 and Occludin. In addition, through high-throughput sequencing, in the probiotic therapy and prophylactic mode, the diversity and composition of the gut microbiota of HP-infected mice were clarified, the potential functions of the gut microbiota were analyzed, the levels of short-chain fatty acids (SCFAs) were measured, and the effects of L. salivarius NCUH062003 on the gut microbiota and its metabolites in HP-infected mice treated with amoxicillin/metronidazole were revealed. This study provides functional strain resources for the development and application of microbial agents seeking to antagonize H. pylori beyond antibiotics. Full article
(This article belongs to the Section Gut Microbiota)
Show Figures

Graphical abstract

Graphical abstract
Full article ">Figure 1
<p>(<b>A</b>) The schematic diagram of <span class="html-italic">H. pylori</span> infection in the multiple therapy and prophylaxis processes conducted on C57BL/6 mice. (<b>B</b>) Schematic diagram showing the mechanisms of <span class="html-italic">L. salivarius</span> NCUH062003. A total of 9 groups were formed, with 8 mice in each group.</p>
Full article ">Figure 2
<p>(<b>A</b>,<b>B</b>) Determination of the abundance of <span class="html-italic">H. pylori</span> in the gastric tissues of mice in therapeutic and prophylactic groups. (<b>C</b>,<b>D</b>) Determination of the urease activity of the mouse gastric mucosa in therapeutic and prophylactic groups. Therapeutic groups: (1) control, (2) HP_NaCl, (3) HP_LP61, (4) HP_LS03, (5) HP_Ant, (6) and Ant_LS03 groups. Prophylactic groups: (1) control, (7) NaCl_HP, (8) LP61_HP, (9) and LS03_HP groups. LP61: <span class="html-italic">L. plantarum</span> CMCC 20261. LS03: <span class="html-italic">L. salivarius</span> NCUH062003 ANT: 0.125 μg mL<sup>−1</sup> amoxicillin and 0.5 μg mL<sup>−1</sup> metronidazole. A total of 9 groups were formed, with 8 mice in each group. Different lowercase letters in the bar graphs indicated significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
Full article ">Figure 3
<p>(<b>A</b>) Histopathology of gastric antrum tissue in the pyloric part of mice from different groups as determined by hematoxylin and eosin staining (200×). (<b>B</b>) Gastric mucosal lymphocyte infiltration score. (<b>C</b>) Gastric mucosal injury score. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups. Black arrow: massive vacuole formation in lamina propria of gastric mucosa. Red arrow: neutrophil and lymphocyte infiltration in epithelial layer and lamina propria; green arrow: erythrocytes and hemorrhage in muscularis mucosa. Different lowercase letters in the bar graphs indicated significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
Full article ">Figure 4
<p>Determination of MPO activity (<b>A</b>,<b>F</b>) and SOD levels (<b>E</b>,<b>J</b>) in gastric tissue of mice and the levels of pro-inflammatory factors IL-1β (<b>B</b>,<b>G</b>) and IL-6 (<b>C</b>,<b>H</b>) and anti-inflammatory factor IL-10 (<b>D</b>,<b>I</b>) in the serum of mice in the prophylactic and therapeutic groups, as determined by enzyme-linked immunosorbent assay (ELISA). Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups. Different lowercase letters in the bar graphs indicated significant differences (<span class="html-italic">p</span> &lt; 0.05).</p>
Full article ">Figure 5
<p>Immunohistochemical staining of pro-inflammatory IL-1β (<b>A</b>) and anti-inflammatory TGF-β (<b>B</b>) in mice gastric tissue in the therapeutic and prophylactic groups (200×). Hematoxylin-stained nuclei were blue, and DAB (3,3′-Diaminobenzidine) showed positive expression in a brownish color. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups.</p>
Full article ">Figure 6
<p>(<b>A</b>) Immunofluorescence heterologous double-labeled Ki-67 and β-catenin staining images in gastric tissues used to assess the apoptosis of gastric epithelial cells. (<b>B</b>) Immunofluorescence homologous double-labeled staining images of Occludin and ZO1 proteins involved in gastric mucosal epithelial repair (400×). DAPI channel nuclei appear blue, 488 channel positivity appears green, and CY3 channel positivity appears red. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups.</p>
Full article ">Figure 7
<p>(<b>A</b>) Alpha diversity index of the mice gut microbiota samples in each therapeutic group: (<b>a</b>) ACE index, (<b>b</b>) Chao1 index, (<b>c</b>) Shannon index, and (<b>d</b>) Simpson index. (<b>B</b>) The PCoA chart of the gut microbiota of mice in each therapeutic group. (<b>C</b>) The hierarchical clustering tree diagram of the gut microbiota of mice in therapeutic groups. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. A total of 6 groups were formed, with 8 mice in each group.</p>
Full article ">Figure 8
<p>(<b>A</b>) The relative abundance of gut microbiota at the phylum level of mice in each therapeutic group. (<b>B</b>) Venn diagram of the gut microbiota of mice in each therapeutic group. (<b>C</b>) The relative abundance of gut microbiota at the genus level of mice in each therapeutic group. The taxonomic cladogram (<b>D</b>) and the histogram (<b>E</b>) from LEfSe analysis of the gut microbiota in therapeutic groups. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. A total of 6 groups were formed, with 8 mice in each group.</p>
Full article ">Figure 9
<p>(<b>A</b>) Alpha diversity index of the mice gut microbiota samples in each prophylactic group: (<b>a</b>) ACE index, (<b>b</b>) Chao1 index, (<b>c</b>) Shannon index, and (<b>d</b>) Simpson index. The beta diversity of gut microbiota of mice in prophylactic groups: (<b>B</b>) PCoA plot and (<b>C</b>) NMDS plot. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups. A total of 4 groups were formed, with 8 mice in each group.</p>
Full article ">Figure 10
<p>(<b>A</b>) The relative abundance of gut microbiota at the phylum level of mice in each prophylactic group. (<b>B</b>) Venn diagram of the gut microbiota of mice in each prophylactic group. (<b>C</b>) The relative abundance of gut microbiota at the genus level of mice in each prophylactic group. The taxonomic cladogram (<b>D</b>) and the histogram (<b>E</b>) from LEfSe analysis of the gut microbiota in prophylactic groups. Prophylactic groups: control, NaCl_HP, LP61_HP, and LS03_HP groups. A total of 4 groups were formed, with 8 mice in each group.</p>
Full article ">Figure 11
<p>(<b>A</b>) Metabolic pathway statistical map for predicted functions of gut microbiota in each therapeutic group. (<b>B</b>) PCoA for potential functional units of the gut microbiota of mice in each therapeutic group. (<b>C</b>) Significantly different metabolic pathways between the HP_Ant and control groups in the predicted functions of gut microbiota. (<b>D</b>) Significantly different metabolic pathways between the Ant_LS03 and control groups in the predicted functions of gut microbiota. Therapeutic groups: control, HP_NaCl, HP_LP61, HP_LS03, HP_Ant, and Ant_LS03 groups. A total of 6 groups were formed, with 8 mice in each group.</p>
Full article ">
19 pages, 1360 KiB  
Article
Non-Helicobacter pylori Helicobacters, a Treatable Provocateur of Parkinson’s Disease: Hypothesis, Evidence and Species Specificity
by Wenjing Wang, Melvyn Smith, Richard Ellis, Antonella Savio, Amanda Nevel, Chianna Umamahesan, Polychronis Pavlidis, Bu’ Hussain Hayee, David Taylor, Allan H. Young, André Charlett, Sylvia M. Dobbs and R. John Dobbs
Int. J. Mol. Sci. 2024, 25(23), 13123; https://doi.org/10.3390/ijms252313123 - 6 Dec 2024
Viewed by 776
Abstract
Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson’s disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD [...] Read more.
Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson’s disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD features can precede the symptomatic onset of motor features by decades. We hypothesise that the non-H. pylori Helicobacters (NHPH), which have farm, companion and wild animals as their main hosts, can have a role in PD aetiopathogenesis. In those occupationally at risk of NHPH infection, we address whether there is increased mortality with PD, or depression or suicide. Our systematic review gave evidence that occupational exposure to animals/their products is associated with excess mortality with PD. Indeed, whilst livestock farming increased the risk, crop farming decreased it. Moreover, excess mortality from non-Hodgkin lymphoma in livestock farmers is compatible with NHPH being causal. Our scoping review showed that farmers, veterinarians and abattoir workers have an increased risk of depression and suicide; whether their depression is associated with being down the pathway to PD and/or the presence of Helicobacter infection needs investigation. Regarding Helicobacter species specificity, the link between the presence of NHPH in gastric biopsy and PD was described using a ureA polymerase chain reaction (PCR) assay, targeting the most-commonly named NHPH, H. suis. We describe its redesign and optimisation as a probe-based PCR, confirming the exclusion of H. pylori but not H. suis specificity (additionally identifying 6 species of a 22-NHPH-species panel). The exploration of the zoonotic hypothesis requires a non-invasive pan-Helicobacter PCR screen, allowing the detection and molecular grouping of Helicobacter species. Full article
Show Figures

Figure 1

Figure 1
<p>Limit of detection experiment for the ureA assay, tested against a tenfold dilution series of H. suis DNA. Cycle threshold (Ct) values are tabulated (<b>above</b>). Amplification plots of a 10-fold dilution series on H. suis DNA samples, containing 2.22 × 10<sup>7</sup> to 2.22 × 10<sup>1</sup> bacterial genome equivalents per reaction, are shown (<b>below</b>). The baseline threshold (horizontal red line) is set at 337800 to optimise signal-to-noise.</p>
Full article ">Figure 2
<p>Flow chart based on PRISMA guidelines for (<b>a</b>) systematic review of mortality associated with idiopathic Parkinsonism in occupations with exposure to animals and/or their products, and (<b>b</b>) scoping review of depression and suicide in occupations with exposure to animals and/or their products.</p>
Full article ">Figure 2 Cont.
<p>Flow chart based on PRISMA guidelines for (<b>a</b>) systematic review of mortality associated with idiopathic Parkinsonism in occupations with exposure to animals and/or their products, and (<b>b</b>) scoping review of depression and suicide in occupations with exposure to animals and/or their products.</p>
Full article ">Figure 3
<p>Summary of the major findings. From the literature review: (i) the association of Parkinson’s disease (PD) deaths with livestock farming; (ii) the excess non-Hodgkin lymphoma in livestock farmers compatible with non-<span class="html-italic">Helicobacter pylori Helicobacter</span> (NHPH) causality; and (iii) the link between gastric NHPH and PD described using PCR, targeting porcine <span class="html-italic">Helicobacter</span>. From the current investigation: the redesign into a probe-based PCR confirmed <span class="html-italic">H. pylori</span> exclusion but showed a lack of specificity within NHPH. Further exploration of the zoonotic hypothesis requires a pan-<span class="html-italic">Helicobacter</span> screen.</p>
Full article ">
31 pages, 3640 KiB  
Review
Helicobacter pylori: Routes of Infection, Antimicrobial Resistance, and Alternative Therapies as a Means to Develop Infection Control
by Ayman Elbehiry, Adil Abalkhail, Nuha Anajirih, Fahad Alkhamisi, Mohammed Aldamegh, Abdullah Alramzi, Riyad AlShaqi, Naif Alotaibi, Abdullah Aljuaid, Hilal Alzahrani, Feras Alzaben, Mohammed Rawway, Mai Ibrahem, Moustafa H. Abdelsalam, Nermin I. Rizk, Mohamed E. A. Mostafa, Moneef Rohail Alfaqir, Husam M. Edrees and Mubarak Alqahtani
Diseases 2024, 12(12), 311; https://doi.org/10.3390/diseases12120311 - 3 Dec 2024
Viewed by 1696
Abstract
Helicobacter pylori (H. pylori) is a Gram-negative, spiral-shaped bacterium that colonizes the gastric epithelium and is associated with a range of gastrointestinal disorders, exhibiting a global prevalence of approximately 50%. Despite the availability of treatment options, H. pylori frequently reemerges and [...] Read more.
Helicobacter pylori (H. pylori) is a Gram-negative, spiral-shaped bacterium that colonizes the gastric epithelium and is associated with a range of gastrointestinal disorders, exhibiting a global prevalence of approximately 50%. Despite the availability of treatment options, H. pylori frequently reemerges and demonstrates increasing antibiotic resistance, which diminishes the efficacy of conventional therapies. Consequently, it is imperative to explore non-antibiotic treatment alternatives to mitigate the inappropriate use of antibiotics. This review examines H. pylori infection, encompassing transmission pathways, treatment modalities, antibiotic resistance, and eradication strategies. Additionally, it discusses alternative therapeutic approaches such as probiotics, anti-biofilm agents, phytotherapy, phototherapy, phage therapy, lactoferrin therapy, and vaccine development. These strategies aim to reduce antimicrobial resistance and enhance treatment outcomes for H. pylori infections. While alternative therapies can maintain low bacterial levels, they do not achieve complete eradication of H. pylori. These therapies are designed to bolster the immune response, minimize side effects, and provide gastroprotective benefits, rendering them suitable for adjunctive use alongside conventional treatments. Probiotics may serve as adjunctive therapy for H. pylori; however, their effectiveness as a monotherapy is limited. Photodynamic and phage therapies exhibit potential in targeting H. pylori infections, including those caused by drug-resistant strains, without the use of antibiotics. The development of a reliable vaccine is also critical for the eradication of H. pylori. This review identifies candidate antigens such as VacA, CagA, and HspA, along with various vaccine formulations, including vector-based and subunit vaccines. Some vaccines have demonstrated efficacy in clinical trials, while others have shown robust immune protection in preclinical studies. Nevertheless, each of the aforementioned alternative therapies requires thorough preclinical and clinical evaluation to ascertain their efficacy, side effects, cost-effectiveness, and patient compliance. Full article
Show Figures

Figure 1

Figure 1
<p>Flow chart explaining the review process for manuscripts that have been screened.</p>
Full article ">Figure 2
<p>The pathways through which <span class="html-italic">H. pylori</span> is transmitted. Person-to-person transmission occurs among children, the elderly, healthcare workers, and individuals living in developing countries. The bacterium can spread through oral–oral, fecal–oral, or gastric–oral routes, as well as through fecal shedding that contaminates food or water sources. Oral–oral transmission may occur when sharing food utensils or between mothers and their newborns. Additionally, <span class="html-italic">H. pylori</span> can be transmitted to animals such as sheep, dogs, cats, and chickens through fecal shedding or direct fecal–oral contact. Food and water sources contaminated with <span class="html-italic">H. pylori</span> can also directly transmit the bacteria to susceptible individuals.</p>
Full article ">Figure 3
<p>The prevalence rates of multidrug-resistant <span class="html-italic">H. pylori</span> across various regions, including Asia (2001–2022), Africa (2007–2017), Europe (2013–2021), and America (2011–2022). The resistance rates to clarithromycin were found to be 37% in Asia, 15% in Africa, 22% in Europe, and 31.5% in America. For metronidazole, the resistance rates were 51% in Asia, 91% in Africa, 27% in Europe, and 42.1% in America. The resistance rates to levofloxacin were reported as 19% in Asia, 14% in Africa, 18% in Europe, and 37.6% in America. Lastly, amoxicillin resistance rates were recorded at 4% in Asia, 38% in Africa, 1% in Europe, and 2.6% in America.Resistance mechanisms primarily stem from mutations that alter pharmacological targets. Drug-resistant genotypes are linked to mutations affecting membrane permeability, biofilm formation, and efflux pumps [<a href="#B120-diseases-12-00311" class="html-bibr">120</a>,<a href="#B128-diseases-12-00311" class="html-bibr">128</a>]. Amoxicillin resistance mainly arises from changes in membrane permeability and mutations in the penicillin-binding protein gene [<a href="#B120-diseases-12-00311" class="html-bibr">120</a>]. <span class="html-italic">H. pylori</span> strains often resist clarithromycin due to point mutations in <span class="html-italic">23S rRNA</span>. A study at Peking University utilized next-generation sequencing to identify genetic factors enhancing resistance to levofloxacin and clarithromycin [<a href="#B129-diseases-12-00311" class="html-bibr">129</a>]. Key mutation sites for clarithromycin resistance include peptidyl transferases in the <span class="html-italic">23S rRNA</span>, with A2143G and A2142G being the most common. Mutations in the DNA gyrase (<span class="html-italic">gyrA</span>) gene (N87K, D91N, D91G) were linked to levofloxacin resistance [<a href="#B129-diseases-12-00311" class="html-bibr">129</a>]. Reduced drug influx due to structural changes in lipopolysaccharide (LPS) membranes also contributes to resistance. Mutations in the <span class="html-italic">rfaF</span> (LPS heptosyltransferase II) gene lead to deep, coarse LPS drug absorption [<a href="#B130-diseases-12-00311" class="html-bibr">130</a>] and causing slight resistance to chloramphenicol, along with cross-resistance to amoxicillin, tetracycline, and clarithromycin [<a href="#B131-diseases-12-00311" class="html-bibr">131</a>]. Increased expression of <span class="html-italic">tolC</span> homolog genes (<span class="html-italic">hefA</span>) in patients with gastrointestinal disorders in Iran [<a href="#B132-diseases-12-00311" class="html-bibr">132</a>] was linked to efflux pump induction, as shown by real-time PCR in metronidazole and clarithromycin-resistant bacteria. The multidrug-resistant phenotype was found in 9.5% of cases. A genome-wide analysis identified prevalent mutations, including A2143G in <span class="html-italic">23S rRNA</span> (63.1%) and alterations in the <span class="html-italic">rdxA</span> gene (85.5%).</p>
Full article ">Figure 4
<p>An overview of the biofilm formation process: (1) Attachment stage of biofilm formation involves reversible and irreversible processes. Reversible attachment occurs when planktonic cells adhere to surfaces via chemical interactions, aided by virulence factors like adhesins and pili, triggering biofilm formation and increasing microbial susceptibility to antimicrobials. (2) Growth (irreversible attachment) leads to microbial proliferation and colony establishment, enhancing adherence through transcriptional changes. This phase promotes substrate exchange, metabolic product distribution, and byproduct excretion. <span class="html-italic">H. pylori</span> secrete EPS, which lower biofilm cell susceptibility to host defenses and antimicrobials. (3) Development features an increasing extracellular matrix around microcolonies, driven by EPS production and quorum-sensing communication, both vital for resistance. Mature biofilms have high EPS content and interstitial spaces for nutrient, water, and planktonic cell movement. (4) Spreading occurs when detachment due to nutrient depletion prompts cells to seek new surfaces through erosion and sloughing.</p>
Full article ">Figure 5
<p>A range of alternative therapeutic approaches has been developed to combat the antimicrobial resistance exhibited by <span class="html-italic">H. pylori</span>. Probiotic therapy employs non-immune mechanisms to counteract <span class="html-italic">H. pylori</span> by competing for attachment sites, inhibiting the expression of virulence genes, and inducing cell death. Additionally, it reduces inflammatory mediators and regulates anti-inflammatory cytokines through immune mechanisms. Photodynamic therapy effectively eradicates <span class="html-italic">H. pylori</span> by generating ROS using a light source in conjunction with a photosensitizer. Phage therapy involves the production of progeny particles from bacteriophages that lyse host cells. The development of vaccines utilizing virulence antigens is crucial for reducing colonization and eradicating <span class="html-italic">H. pylori</span>. Phytotherapy can inhibit urease activity, prevent bacterial adhesion, and enhance membrane permeation against <span class="html-italic">H. pylori</span> infection. Lactoferrin therapy sequesters iron, interacts with lipopolysaccharides and lipoteichoic acids, modulates serine protease activity, and engages with peptidoglycan, ultimately leading to the collapse of the cellular wall.</p>
Full article ">
16 pages, 1094 KiB  
Article
Prevalence of Abnormalities at Tandem Endoscopy in Patients Referred for Colorectal Cancer Screening/Surveillance Colonoscopy
by George Triadafilopoulos
Cancers 2024, 16(23), 3998; https://doi.org/10.3390/cancers16233998 - 29 Nov 2024
Viewed by 714
Abstract
Introduction: Performing a tandem endoscopy and colonoscopy in selected individuals has advantages, such as the early detection of benign and/or precancerous foregut diseases; it is efficient, and it may allow added therapies. It may also have disadvantages, such as generating anxiety from false-positive [...] Read more.
Introduction: Performing a tandem endoscopy and colonoscopy in selected individuals has advantages, such as the early detection of benign and/or precancerous foregut diseases; it is efficient, and it may allow added therapies. It may also have disadvantages, such as generating anxiety from false-positive screening, possible harm from further testing, and unproven cost-effectiveness. Aims: We aimed to examine the prevalence of foregut endoscopic and histologic abnormalities in subjects referred for screening/surveillance colonoscopy who also underwent a tandem endoscopy. We wanted to (1) assess implications for cancer detection, intervention, and surveillance of precancerous foregut abnormalities, (2) identify benign foregut lesions, and (3) generate data on the utilities of this tandem approach. Patients and Methods: A retrospective cohort study of consecutive subjects referred for screening or surveillance colonoscopy who also underwent an endoscopy. Based on national screening guidelines, responses to prompting questions, personal or family history, or other risk factors, subjects were assigned to tandem endoscopy with biopsies (modified Seattle and Sydney protocols), under one anesthesia. Results: Of the 1004 patients referred for colonoscopy, 317 (32%) underwent tandem endoscopy. There were 214 women and 103 men. There were 237 Whites, 16 Asians, 40 Blacks, and 24 Hispanics. Median age was 59 (range 19–85). At endoscopy, we identified actionable benign (45%) peptic, inflammatory, and H. pylori-related abnormalities, and premalignant findings (i.e., intestinal metaplasia, 27%, dysplasia, 2%, and cancer 0.9%), comparable to the premalignant (40.3%) and malignant (0.6%) colonoscopy yield. Conclusions: When implemented based on national screening guidelines, tandem EGD and colonoscopy combines Barrett’s esophagus and gastric cancer screening in one examination, and it has a high yield in a diverse US population. Full article
(This article belongs to the Collection Oncology: State-of-the-Art Research in the USA)
Show Figures

Figure 1

Figure 1
<p>Study flow diagram.</p>
Full article ">Figure 2
<p>Need for action depending on endoscopic and histologic findings at endoscopy in the 317 subjects of the dual EGD/colonoscopy cohort.</p>
Full article ">Figure 3
<p>Point % prevalence of key benign and malignant endoscopic abnormalities at tandem EGD and colonoscopy in 317 subjects. PD: Peptic duodenitis; PS: Pyloric Stenosis; G: Gastritis; AN: Antral Nodule; FP: Fundic Polyp; Cancer; HH: Hiatal Hernia; SR: Schatzki’s Ring; EE: Erosive Esophagitis; BE: Barrett’s Esophagus; EoE: Eosinophilic Esophagitis; Polyps; CRC: Colorectal Cancer.</p>
Full article ">Figure 4
<p>Point % prevalence of key histologic abnormalities at tandem EGD and colonoscopy in 317 subjects. DL: Duodenal lymphocytosis; HP+: Active <span class="html-italic">H. pylori</span> infection; GIM: Gastric Intestinal Metaplasia; SCJ-IM: Squamocolumnar Junction–Intestinal Metaplasia; PAM: Pancreatic Acinar Metaplasia; Cancer; PE: Peptic esophagitis; EoE: Eosinophilic esophagitis; TA: Tubular Adenoma (including serrated polyps); HP: Hyperplastic polyps; CRC: Colorectal cancer.</p>
Full article ">
Back to TopTop