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Among these secondary colonizers,\n                      <jats:italic toggle=\"yes\">Fusobacterium<\/jats:italic>\n                      species have documented associations with several gastrointestinal cancers. We found that both\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">F. nucleatum<\/jats:italic>\n                      invade cultured human gastric adenocarcinoma cells, but\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      exhibited higher adherence and invasion, and hypoxic conditions promoted higher bacterial survival. Both adherence and invasion were inhibited by exogenous GalNAc, a glycan commonly observed in membrane glycoproteins of adenocarcinoma cells and a target of the fusobacterial adhesin Fap2. Using a mouse model of stomach metaplasia, we found that\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      colonized gastric tissue only after metaplasia onset, growing in multispecies biofilms in the mucus layer, while\n                      <jats:italic toggle=\"yes\">F. nucleatum<\/jats:italic>\n                      colonized neither healthy nor metaplastic gastric tissue. Metaplasia led to upregulation of Gal-GalNAc in the stomach, and reduced gastric acidity allowed higher\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      loads in this model. By contrast, inflammation and the presence of\n                      <jats:italic toggle=\"yes\">H. pylori<\/jats:italic>\n                      did not significantly influence stomach colonization by\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      . Further assessment of additional\n                      <jats:italic toggle=\"yes\">Fusobacterium<\/jats:italic>\n                      species and strains revealed that whereas all tested species can invade gastric cancer cells\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      , only\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">F. polymorphum<\/jats:italic>\n                      robustly colonize the metaplastic gastric tissue of the mouse model similar to\n                      <jats:italic toggle=\"yes\">F. animalis<\/jats:italic>\n                      . Overall, our data support a model in which\n                      <jats:italic toggle=\"yes\">H. pylori<\/jats:italic>\n                      -induced metaplasia makes the stomach susceptible to secondary infection by other cancer-associated microbes, including some\n                      <jats:italic toggle=\"yes\">Fusobacterium<\/jats:italic>\n                      species.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        <jats:italic toggle=\"yes\">Helicobacter pylori<\/jats:italic>\n                        infection is the primary risk factor for gastric cancer worldwide, yet the underlying cancer-promoting mechanisms are not fully defined. Our study shows that metaplasia, a precancerous condition typically triggered by\n                        <jats:italic toggle=\"yes\">H. pylori<\/jats:italic>\n                        and characterized by specific changes in gene expression and tissue remodeling, can enable secondary infection by other cancer-associated bacteria. Specifically, we found that certain species of the genus\n                        <jats:italic toggle=\"yes\">Fusobacterium<\/jats:italic>\n                        , linked to several gastrointestinal cancers, colonize the stomach only after the onset of metaplasia. Metaplasia-associated changes in the stomach include altered surface sugars and reduced acidity, which together may create a more permissive environment for bacterial growth. Our findings support a model in which disruptions of gastric tissue architecture induced by chronic\n                        <jats:italic toggle=\"yes\">H. pylori<\/jats:italic>\n                        infection facilitate colonization by other cancer-related bacteria, contributing to the growing body of evidence highlighting the role of bacteria in cancer development.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01747-26","type":"journal-article","created":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T13:00:31Z","timestamp":1791550831000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Metaplasia creates a permissive niche for select\n                    <i>Fusobacterium<\/i>\n                    species in the stomach"],"prefix":"10.1128","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4971-8999","authenticated-orcid":false,"given":"Camilo","family":"G\u00f3mez-Garz\u00f3n","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/007ps6h72","id-type":"ROR","asserted-by":"publisher"}],"name":"Human Biology Division, Fred Hutchinson Cancer Center","place":["Seattle, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0502-2690","authenticated-orcid":false,"given":"Valerie P.","family":"O\u2019Brien","sequence":"additional","affiliation":[{"name":"Borch Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University","place":["West Lafayette, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0183-0025","authenticated-orcid":false,"given":"Qiwen","family":"Chen","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/007ps6h72","id-type":"ROR","asserted-by":"publisher"}],"name":"Human Biology Division, Fred Hutchinson Cancer Center","place":["Seattle, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7763-8465","authenticated-orcid":false,"given":"Katherine S.","family":"Garman","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00py81415","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Gastroenterology, Department of Medicine, Duke University","place":["Durham, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2762-1424","authenticated-orcid":false,"given":"Nina R.","family":"Salama","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/007ps6h72","id-type":"ROR","asserted-by":"publisher"}],"name":"Human Biology Division, Fred Hutchinson Cancer Center","place":["Seattle, USA"]},{"id":[{"id":"https:\/\/ror.org\/00cvxb145","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, University of Washington","place":["Seattle, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","published-online":{"date-parts":[[2026,10,9]]},"reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.3322\/caac.21834"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S2214-109X(19)30488-7"},{"key":"e_1_3_5_4_2","first-page":"3554","article-title":"A human model of gastric carcinogenesis","volume":"48","author":"Correa P","year":"1988","unstructured":"Correa P. 1988. 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