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-? 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.

SUBMITTER: Disson O 

PROVIDER: S-EPMC6219733 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature