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Background  Intestinal fibrosis is a frequent complication of Crohn’s disease. However, the factors that cause chronicity and promote fibrogenesis are not yet understood.    Aims  In the present study, we evaluated the profibrotic effects of adherent-invasive  Escherichia coli  (AIEC) LF82 strain and  Candida albicans  in the gut.    Methods  Colonic fibrosis was induced in C57BL/6 mice by administration of three cycles of 2.5% (w/v) dextran sulfate sodium (DSS) for 5 weeks. LF82 and  C. albicans  were administered orally once at the start of each week or each cycle, respectively. Expression of markers of myofibroblast activation was determined in TGF-β1-stimulated human intestinal epithelial cells (IECs).    Results  LF82 administration exacerbated fibrosis in DSS-treated mice, revealed by increased colonic collagen deposition and expression of the profibrotic genes  Col1a1 ,  Col3a1 ,  Fn1  and  Vim . This was accompanied by enhanced gene expression of proinflammatory cytokines and chemokines, as well as more recruited inflammatory cells into the intestine. LF82 also potentiated TGF-β1-stimulated epithelial–mesenchymal transition and myofibroblast activation in IECs, by further inducing gene expression of the main mesenchymal cell markers  FN1  and  VIM  and downregulating the IEC marker  OCLN . Proinflammatory cytokines were overexpressed with LF82 in TGF-β1-stimulated IECs. Conversely,  C. albicans  did not affect intestinal fibrosis progression in DSS-treated mice or myofibroblast activation in TGF-β1-stimulated IECs.    Conclusions  These results demonstrate that AIEC strain LF82, but not  C. albicans , may play a major profibrogenic role in the gut.

Adherent invasive Escherichia coli (AIEC) strain LF82, but not Candida albicans, plays a profibrogenic role in the intestine