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Peyer’s patch myeloid cells infection by Listeria signals through gp38 + stromal cells and locks intestinal villus invasion

Abstract : 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-γ 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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Submitted on : Tuesday, May 28, 2019 - 4:36:43 PM
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Olivier Disson, Camille Bleriot, Jean-Marie Jacob, Nicolas Serafini, Sophie Dulauroy, et al.. Peyer’s patch myeloid cells infection by Listeria signals through gp38 + stromal cells and locks intestinal villus invasion. Journal of Experimental Medicine, Rockefeller University Press, 2018, 215 (11), pp.2936-2954. ⟨10.1084/jem.20181210⟩. ⟨pasteur-02142521⟩

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