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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\u2019s 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-\u03b3 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.<\/jats:p>","DOI":"10.1084\/jem.20181210","type":"journal-article","created":{"date-parts":[[2018,10,24]],"date-time":"2018-10-24T14:28:20Z","timestamp":1540391300000},"page":"2936-2954","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":54,"title":["Peyer\u2019s patch myeloid cells infection by <i>Listeria<\/i> signals through gp38+ stromal cells and locks intestinal villus invasion"],"prefix":"10.1084","volume":"215","author":[{"given":"Olivier","family":"Disson","sequence":"first","affiliation":[{"name":"Institut Pasteur, Biology of Infection Unit, Paris, France 1"},{"name":"Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale U1117, Paris, France 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