The global stress response regulatorin an adherent-invasivestrain attenuates experimental colitis.

Abstract

Crohn's disease and ulcerative colitis in humans and experimental immune-mediated colitis in mice are likely due in part to overactive immune responses to resident intestinal bacteria, including certain strains of adherent-invasive() such asNC101. We have previously shown that specificNC101 stress responses are upregulated during experimental colitis and attenuate inflammation. However, the roles of broader stress response pathways inNC101 during experimental colitis are unknown. We hypothesize that the global stress response regulator in,, also reduces experimental colitis. We show that intestinalNC101 upregulateexpression during colitis in monocolonized interleukin-10 deficient mice. Furthermore, we demonstrate that-sufficientNC101 have decreased motility and biofilm formationand attenuated intestinal translocation and colitogenic potentialcompared withdeficient. These data suggest that activation of a generalizedstress response,, reduces experimental colitis and may be a potential therapeutic target.