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Kumar, Pawan; Monin, Leticia; Castillo, Patricia; Elsegeiny, Waleed; Horne, William; Eddens, Taylor; Vikram, Amit; Good, Misty; Schoenborn, Alexi A.; Bibby, Kyle; Montelaro, Ronald C.; Metzger, Dennis W.; Gulati, Ajay S.; Kolls, Jay K.
Immunity, 03/2016, Volume: 44, Issue: 3Journal Article
Interleukin-17 (IL-17) and IL-17 receptor (IL-17R) signaling are essential for regulating mucosal host defense against many invading pathogens. Commensal bacteria, especially segmented filamentous bacteria (SFB), are a crucial factor that drives T helper 17 (Th17) cell development in the gastrointestinal tract. In this study, we demonstrate that Th17 cells controlled SFB burden. Disruption of IL-17R signaling in the enteric epithelium resulted in SFB dysbiosis due to reduced expression of α-defensins, Pigr, and Nox1. When subjected to experimental autoimmune encephalomyelitis, IL-17R-signaling-deficient mice demonstrated earlier disease onset and worsened severity that was associated with increased intestinal Csf2 expression and elevated systemic GM-CSF cytokine concentrations. Conditional deletion of IL-17R in the enteric epithelium demonstrated that there was a reciprocal relationship between the gut microbiota and enteric IL-17R signaling that controlled dysbiosis, constrained Th17 cell development, and regulated the susceptibility to autoimmune inflammation. •SFB-induced Th17 cell expansion in the gut controls the degree of SFB colonization•IL-17R-dependent regulation of α-defensin, Nox1, and Pigr controls SFB•Intestinal IL-17R signaling regulates dysbiosis and autoimmune inflammation. Segmented filamentous bacteria (SFB) regulate Th17 cell development in the gastrointestinal tract. Kolls and colleagues find that intestinal IL-17R signaling regulates the abundance of the gut microbiota and SFB specifically by promoting expression of antimicrobial factors. Abrogation of intestinal IL-17R signaling results in bacterial overgrowth and enhanced susceptibility to autoimmune inflammation.
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