Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 215, Issue 11, Pages 2936-2954Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20181210
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Funding
- Institut Pasteur
- Institut National de la Sante et de la Recherche Medicale
- Institut Carnot Pasteur Microbes et Sante
- LabEx IBEID
- European Research Council
- Agence Nationale de Recherche Organolist
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The foodborne pathogen Listeria monocytogenes (Lm) crosses the intestinal villus epithelium via goblet cells (GCs) upon the interaction of Lm surface protein InlA with its receptor E-cadherin. Here, we show that Lm infection accelerates intestinal villus epithelium renewal while decreasing the number of GCs expressing luminally accessible E-cadherin, thereby locking Lm portal of entry. This novel innate immune response to an enteropathogen is triggered by the infection of Peyer's patch CX3CR1(+) cells and the ensuing production of IL-23. It requires STAT3 phosphorylation in epithelial cells in response to IL-22 and IL-11 expressed by lamina propria gp38(+) stromal cells. Lm-induced IFN-gamma signaling and STAT1 phosphorylation in epithelial cells is also critical for Lm-associated intestinal epithelium response. GC depletion also leads to a decrease in colon mucus barrier thickness, thereby increasing host susceptibility to colitis. This study unveils a novel innate immune response to an enteropathogen, which implicates gp38(+) stromal cells and locks intestinal villus invasion, but favors colitis.
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