<i>Alcaligenes faecalis</i> promotes colitis to colorectal cancer transition through IgA+ B cell suppression and vinculin acetylation

Lymphoid tissue-resident commensal bacteria (LRC), a subtype of gut microbiota essential for inflammation-associated carcinogenesis, predominantly attribute to colorectal cancer(CRC), whereas its role was largely unknown. Herein, we found <i>Alcaligenes faecalis</i> (<i>A. faecalis</i>), the main LRC embedded in Peyer's patches, was abundantly enriched in colitis, adenoma, and stage-dependently observed in CRC tissues. Interestingly, <i>A. faecalis</i> alone can not affect intestinal homeostasis, while during colitis, <i>A. faecalis</i> significantly translocated from Peyer's patches to colon, remarkably attenuated immune response abilities of B cells, T cells, and DC cells in PPs, consequently impeded IgA+ B cells homing. Meanwhile, during colitis, the ectopia of <i>A. faecalis</i> in colon tissues, promoted vinculin acetylation by <i>A. faecalis</i>-derived metabolite acetic acid, which impeded intestinal barrier via hindering the binding of vinculin to β-catenin. Our study revealed <i>A. faecalis</i> not only suppress mucosal immune responses via reducing IgA+ B cells in Peyer's patches but also disrupt intestinal barrier via increasing vinculin acetylation, ultimately promoting inflammation-to-cancer transition in CRC.