 |
Journal articles
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.
Cited literature [99 references]
https://hal-pasteur.archives-ouvertes.fr/pasteur-02142521
Contributor : Andrée Diakite <>
Submitted on : Tuesday, May 28, 2019 - 4:36:43 PM
Last modification on : Tuesday, June 22, 2021 - 3:42:10 PM
Contributor : Andrée Diakite <>
Submitted on : Tuesday, May 28, 2019 - 4:36:43 PM
Last modification on : Tuesday, June 22, 2021 - 3:42:10 PM
File
JEM_20181210.pdf
Publication funded by an institution
Licence
Distributed under a Creative Commons Attribution - NonCommercial - ShareAlike 4.0 International License