| First Author | Disson O | Year | 2018 |
| Journal | J Exp Med | Volume | 215 |
| Issue | 11 | Pages | 2936-2954 |
| PubMed ID | 30355616 | Mgi Jnum | J:269099 |
| Mgi Id | MGI:6272942 | Doi | 10.1084/jem.20181210 |
| Citation | Disson O, et al. (2018) Peyer's patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion. J Exp Med 215(11):2936-2954 |
| abstractText | 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. |
