Peyer's patch myeloid cells infection by signals through gp38 stromal cells and locks intestinal villus invasion.

The foodborne pathogen () crosses the intestinal villus epithelium via goblet cells (GCs) upon the interaction of surface protein InlA with its receptor E-cadherin. Here, we show that infection accelerates intestinal villus epithelium renewal while decreasing the number of GCs expressing luminally accessible E-cadherin, thereby locking 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. -induced IFN-γ signaling and STAT1 phosphorylation in epithelial cells is also critical for -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.