Yersiniabactin-Producing Adherent/Invasive Escherichia coli Promotes Inflammation-Associated Fibrosis in Gnotobiotic Mice.

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ID: 79842
2019
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Abstract
Fibrosis is a significant complication of intestinal disorders associated with microbial dysbiosis and pathobiont expansion, notably Crohn's disease (CD). Mechanisms that favor fibrosis are not well understood, and therapeutic strategies are limited. Here we demonstrate that colitis-susceptible -deficient mice develop inflammation-associated fibrosis when monoassociated with adherent/invasive (AIEC) that harbors the yersiniabactin (Ybt) pathogenicity island. Inactivation of Ybt siderophore production in AIEC nearly abrogated fibrosis development in inflamed mice. In contrast, inactivation of Ybt import through its cognate receptor FyuA enhanced fibrosis severity. This corresponded with increased colonic expression of profibrogenic genes prior to the development of histological disease, therefore suggesting causality. -deficient AIEC also exhibited greater localization within subepithelial tissues and fibrotic lesions that was dependent on Ybt biosynthesis and corresponded with increased fibroblast activation Together, these findings suggest that Ybt establishes a profibrotic environment in the host in the absence of binding to its cognate receptor and indicate a direct link between intestinal AIEC and the induction of inflammation-associated fibrosis.
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ellermann2019yersiniabactinproducinginfection Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Ellermann, Melissa;Gharaibeh, Raad Z;Fulbright, Laura;Dogan, Belgin;Moore, Lyndsey N;Broberg, Christopher A;Lopez, Lacey R;Rothemich, Aaron M;Herzog, Jeremy W;Rogala, Allison;Gordon, Ilyssa O;Rieder, Florian;Brouwer, Cory R;Simpson, Kenneth W;Jobin, Christian;Sartor, R Balfour;Arthur, Janelle C;
Journal Infection and immunity
Year 2019
DOI
e00587-19
URL
Keywords
crohn’s disease microbiota fibrosis microbiome colitis intestinal inflammation aiec yersiniabactin

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