{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T16:32:20Z","timestamp":1789576340900,"version":"build-2803163510"},"reference-count":40,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2023,8,17]],"date-time":"2023-08-17T00:00:00Z","timestamp":1692230400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      The present study aims to investigate the effect of\n                      <jats:italic>Helicobacter pylori<\/jats:italic>\n                      (Hp) infection on gastric mucosal microbiota in patients with chronic gastritis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Here recruited a population of 193 patients with both chronic gastritis and positive rapid urease, including 124 patients with chronic atrophic gastritis (CAG) and 69 patients with chronic non-atrophic gastritis (nCAG). Immunoblotting was used to detect four serum Hp antibodies (UreA, UreB, VacA and CagA) to determine the types of virulent Hp-I and avirulent Hp-II infections. Gastric microbiota was profiled by 16S rRNA gene V3-V4 region, and R software was used to present the relationship between the microbial characteristics and the type of Hp infection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In the stomach of patients with Hp-positive gastritis, the dominant gastric bacterial genera included\n                      <jats:italic>Ralstonia<\/jats:italic>\n                      (23.94%),\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      (20.28%),\n                      <jats:italic>Pseudonocardia<\/jats:italic>\n                      (9.99%),\n                      <jats:italic>Mesorhizobium<\/jats:italic>\n                      (9.21%),\n                      <jats:italic>Bradyrhizobium<\/jats:italic>\n                      (5.05%), and\n                      <jats:italic>Labrys<\/jats:italic>\n                      (4.75%). The proportion of Hp-I infection was significantly higher in CAG patients (91.1%) than in nCAG patients (71.0%) (\n                      <jats:italic>P<\/jats:italic>\n                      &amp;lt; 0.001). The gastric microbiota richness index (observed OTUs, Chao) was significantly lower in CAG patients than in nCAG patients (\n                      <jats:italic>P &amp;lt;<\/jats:italic>\n                      0.05). Compared with avirulent Hp-II infection, virulent Hp-I infection significantly decreased the Shannon index in CAG patients (\n                      <jats:italic>P &amp;lt;<\/jats:italic>\n                      0.05). In nCAG patients, Hp-I infected patients had lower abundances of several dominant gastric bacteria (\n                      <jats:italic>Aliidiomarina<\/jats:italic>\n                      ,\n                      <jats:italic>Reyranella<\/jats:italic>\n                      ,\n                      <jats:italic>Halomonas<\/jats:italic>\n                      ,\n                      <jats:italic>Pseudomonas<\/jats:italic>\n                      ,\n                      <jats:italic>Acidovorax<\/jats:italic>\n                      ) than Hp-II infected patients. Meanwhile, in CAG patients, Hp-I infected patients occupied lower abundances of several dominant oral bacteria (\n                      <jats:italic>Neisseria<\/jats:italic>\n                      ,\n                      <jats:italic>Staphylococcus<\/jats:italic>\n                      and\n                      <jats:italic>Haemophilus<\/jats:italic>\n                      ) than Hp-II infected patients. In addition, bile reflux significantly promoted the colonization of dominant oral microbiota (\n                      <jats:italic>Veillonella<\/jats:italic>\n                      ,\n                      <jats:italic>Prevotella 7<\/jats:italic>\n                      and\n                      <jats:italic>Rothia<\/jats:italic>\n                      ) in the stomach of CAG patients. There was no significant symbiotic relationship between\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria and non-\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria in the stomach of nCAG patients, while\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria distinctly linked with the non-\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria (\n                      <jats:italic>Pseudolabrys<\/jats:italic>\n                      ,\n                      <jats:italic>Ralstonia<\/jats:italic>\n                      ,\n                      <jats:italic>Bradyrhizobium<\/jats:italic>\n                      ,\n                      <jats:italic>Mesorhizobium<\/jats:italic>\n                      and\n                      <jats:italic>Variovorax<\/jats:italic>\n                      ) in CAG patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Virulent Hp infection alters the gastric microbiota, reduces microbial diversity, and enhances the symbiotic relationship between the\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria and non-\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      bacteria in patients with chronic gastritis. The data provides new evidence for treating Hp infection by improving the gastric microbiota.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcimb.2023.1221433","type":"journal-article","created":{"date-parts":[[2023,8,18]],"date-time":"2023-08-18T03:04:03Z","timestamp":1692327843000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":29,"title":["Helicobacter pylori infection altered gastric microbiota in patients with chronic gastritis"],"prefix":"10.3389","volume":"13","author":[{"given":"Zhaolai","family":"Hua","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Le","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiahui","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jianping","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenfeng","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qihai","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junfeng","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2023,8,17]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.3389\/fmicb.2021.713955","article-title":"Helicobacter pylori in human stomach: The inconsistencies in clinical outcomes and the probable causes","volume":"12","author":"Alexander","year":"2021","journal-title":"Front. 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