{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,27]],"date-time":"2026-10-27T19:38:47Z","timestamp":1793129927078,"version":"4.5.0"},"reference-count":71,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T00:00:00Z","timestamp":1791936000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["K08 DK-123316"],"award-info":[{"award-number":["K08 DK-123316"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000861","name":"Burroughs Wellcome Fund","doi-asserted-by":"publisher","award":["G-1020904.01"],"award-info":[{"award-number":["G-1020904.01"]}],"id":[{"id":"10.13039\/100000861","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["T32 AI007520"],"award-info":[{"award-number":["T32 AI007520"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000011","name":"Howard Hughes Medical Institute","doi-asserted-by":"publisher","award":["Emerging Pathogens Initiative"],"award-info":[{"award-number":["Emerging Pathogens Initiative"]}],"id":[{"id":"10.13039\/100000011","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,10,14]]},"abstract":"ABSTRACT<\/jats:title>\n \n \n \n Adherent-invasive\n Escherichia coli<\/jats:italic>\n (AIEC) are strongly implicated in the pathogenesis of Crohn\u2019s disease, but the virulence factors driving their invasive and pro-inflammatory behavior remain incompletely defined. Here, we demonstrate that vitamin B\n 12<\/jats:sub>\n availability modulates\n pdu<\/jats:italic>\n -dependent AIEC virulence. The 1,2-propanediol utilization (\n pdu<\/jats:italic>\n ) operon, which requires vitamin B\n 12<\/jats:sub>\n as a cofactor, has previously been associated with bacterial virulence. Here, we validated this association and demonstrated its functional relevance in mouse models of colitis. Deletion of\n pduB<\/jats:italic>\n , a structural component of the\n pdu<\/jats:italic>\n microcompartment, in the prototypical AIEC strain NRG857c impaired invasion of intestinal epithelial cells without affecting bacterial growth, biofilm formation, or intestinal colonization. In contrast,\n pduB<\/jats:italic>\n deletion reduced mucosal association and significantly attenuated colitis in\n \n Il10\n \u2212\/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice. Moreover, loss of\n pduB<\/jats:italic>\n protected against AIEC-induced epithelial barrier dysfunction and reduced expression of pro-inflammatory cytokines, including\n Il6<\/jats:italic>\n ,\n Il1b<\/jats:italic>\n , and\n Tnf-a<\/jats:italic>\n . Unexpectedly,\n pduB<\/jats:italic>\n deletion was associated with elevated host serum vitamin B\n 12<\/jats:sub>\n levels, and exogenous vitamin B\n 12<\/jats:sub>\n supplementation directly inhibited AIEC invasion\n in vitro<\/jats:italic>\n and effectively protected\n \n Il10\n \u2212\/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice from AIEC-induced colitis. Furthermore, vitamin B\n 12<\/jats:sub>\n -mediated suppression of AIEC invasion and barrier dysfunction was dependent on an intact\n pdu<\/jats:italic>\n pathway. Together, these findings establish\n pduB<\/jats:italic>\n as a key regulator of AIEC virulence. Our findings identify vitamin B\n 12<\/jats:sub>\n availability as a host-modifiable factor that influences AIEC pathogenicity, suggesting potential therapeutic strategies for AIEC-driven intestinal inflammation in Crohn\u2019s disease.\n <\/jats:p>\n <\/jats:sec>\n \n IMPORTANCE<\/jats:title>\n \n In this study, we demonstrated that vitamin B\n 12<\/jats:sub>\n availability modulates a metabolic interaction between adherent-invasive\n Escherichia coli<\/jats:italic>\n (AIEC) and the host micronutrient vitamin B\n 12<\/jats:sub>\n that influences AIEC epithelial invasion. We confirm that a gene within the 1,2-propanediol utilization pathway (\n pduB<\/jats:italic>\n ) is critical for AIEC invasion and the development of intestinal inflammation in multiple mouse models. We further identify that vitamin B\n 12<\/jats:sub>\n , a cofactor for metabolic reactions within the Pdu microcompartment, is altered in the host during infection, suggesting changes in the microbe-host vitamin B\n 12<\/jats:sub>\n utilization dynamics. Functionally, we also show that vitamin B\n 12<\/jats:sub>\n supplementation significantly inhibited AIEC invasion of epithelial cells\n in vitro.<\/jats:italic>\n Lastly, we found that vitamin B\n 12<\/jats:sub>\n supplementation provided strong protection against AIEC-induced colitis in\n \n Il10\n \u2212\/<\/jats:sup>\n <\/jats:italic>\n \u2212<\/jats:sup>\n mice, preventing weight loss, rectal prolapse, tissue damage, and inflammatory infiltration, even in animals colonized with wild-type AIEC. Broadly, our work highlights vitamin B\n 12<\/jats:sub>\n availability as a modifiable host factor that influences AIEC pathogenicity and suggests new therapeutic avenues for therapeutic strategies targeting microbe-nutrient interactions in inflammatory bowel disease.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1128\/mbio.01698-26","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T13:00:16Z","timestamp":1789563616000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Adherent-invasive\n Escherichia coli pduB<\/i>\n drives vitamin B\n 12<\/sub>\n -dependent colitis in mice"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3052-932X","authenticated-orcid":true,"given":"Shahanshah","family":"Khan","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jungyeon","family":"Kim","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Lafrance","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sydney","family":"Field","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center","place":["Dallas, USA"]},{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Li","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Division of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3041-2615","authenticated-orcid":true,"given":"Lisa N.","family":"Kinch","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin J.","family":"Forsberg","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamia A.","family":"Harris-Tryon","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Dermatology, University of Texas Southwestern Medical Center","place":["Dallas, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qian","family":"Cong","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Eugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center","place":["Dallas, USA"]},{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biophysics, University of Texas Southwestern Medical Center","place":["Dallas, USA"]},{"id":[{"id":"https:\/\/ror.org\/05byvp690","id-type":"ROR","asserted-by":"publisher"}],"name":"Harold C. 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