Journal
CELL REPORTS
Volume 15, Issue 8, Pages 1743-1756Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2016.04.049
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Funding
- DFG clinical research unit [KFO257 (TP1)]
- Interdisciplinary Centre for Clinical Research (IZKF) of the University Erlangen-Nurnberg
- European Community's IMI initiative
- German Research Foundation DFG [SPP1656]
- collaborative research centers [SFB 1181 (A08, C05), SFB796 (B07, B09), BE3686/2]
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The intestinal epithelium constitutes an efficient barrier against the microbial flora. Here, we demonstrate an unexpected function of IL-33 as a regulator of epithelial barrier functions. Mice lacking IL-33 showed decreased Paneth cell numbers and lethal systemic infection in response to Salmonella typhimurium. IL-33 was produced upon microbial challenge by a distinct population of pericryptal fibroblasts neighboring the intestinal stem cell niche. IL-33 programmed the differentiation of epithelial progenitors toward secretory IEC including Paneth and goblet cells. Finally, IL-33 suppressed Notch signaling in epithelial cells and induced expression of transcription factors governing differentiation into secretory IEC. In summary, we demonstrate that gut pericryptal fibroblasts release IL-33 to translate bacterial infection into an epithelial response to promote antimicrobial defense.
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