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We investigated the pathogenic factors of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      and their interactions with the gastric microbiome in a population with low gastric cancer but high gastritis rates in Indonesia.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The study included 66\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010positive gastric biopsies. DNA was extracted from the bacterial cultures to examine the pathogenic factors of\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      . The 16S rRNA V3\u2013V4 region was sequenced using next\u2010generation sequencing. The microbiome analysis concentrated on \u03b1\u2010diversity and \u03b2\u2010diversity, along with absolute and relative abundances. Correlation analysis and predicted functional inference were conducted using SECOM and PICRUSt2.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      predominates in\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      \u2010infected stomachs, limiting other bacteria. Although \u03b1\u2010diversity was non\u2010significant, virulent\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      genotypes showed greater microbial diversity, suggesting co\u2010colonization by other taxa. Some taxa were notably abundant across pathogenic subtypes (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05), such as\n                      <jats:italic>Veillonella<\/jats:italic>\n                      sp. in East Asian\u2010type CagA\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      and\n                      <jats:italic>Klebsiella<\/jats:italic>\n                      without\n                      <jats:italic>babB<\/jats:italic>\n                      . The \u03b2\u2010diversity results indicated that microbial diversity and abundance varied according to polymorphisms in patients with different\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      CagA types,\n                      <jats:italic>sabA<\/jats:italic>\n                      status,\n                      <jats:italic>homA\/B<\/jats:italic>\n                      , and\n                      <jats:italic>iceA<\/jats:italic>\n                      subtypes (PERMANOVA test;\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05).\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>H. pylori<\/jats:italic>\n                      <\/jats:styled-content>\n                      dominance remains unchanged when atrophy worsens, alongside decreased microbial diversity (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.05 for atrophy stage 0 vs. stages 1 and 2). Microbial correlation analysis revealed that\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      only had a positive linear relationship with\n                      <jats:italic>Veillonella<\/jats:italic>\n                      (SECOM(Pearson2)\u2009=\u20090.51, SECOM(Distance)\u2009=\u20090.60), whereas\n                      <jats:italic>Streptococcus<\/jats:italic>\n                      sp. correlated with several gastric taxa. Predicted functional inference showed several pathways to be depleted when atrophy progresses.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Various pathogenic factors impact microbial diversity, and bacteria cohabiting in the gastric environment might shape disease outcomes. Additionally, our study uncovers relationships among genera present in the stomach. More research is needed to explore how non\u2010\n                      <jats:italic>Helicobacter<\/jats:italic>\n                      species induce or possibly safeguard against gastric pathologies.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/hel.70072","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T04:10:42Z","timestamp":1758514242000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["<i>Helicobacter pylori<\/i>\n                    Pathogenic Factors and Their Interactions With the Gastric Microbiome"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4439-7073","authenticated-orcid":false,"given":"Camilia Metadea Aji","family":"Savitri","sequence":"first","affiliation":[{"name":"Department of Environmental and Preventive Medicine Oita University Faculty of Medicine  Yufu Oita 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