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Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion

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 numbe...

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Autores principales: Disson, Olivier, Blériot, Camille, Jacob, Jean-Marie, Serafini, Nicolas, Dulauroy, Sophie, Jouvion, Grégory, Fevre, Cindy, Gessain, Grégoire, Thouvenot, Pierre, Eberl, Gérard, Di Santo, James P., Peduto, Lucie, Lecuit, Marc
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219733/
https://www.ncbi.nlm.nih.gov/pubmed/30355616
http://dx.doi.org/10.1084/jem.20181210
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author Disson, Olivier
Blériot, Camille
Jacob, Jean-Marie
Serafini, Nicolas
Dulauroy, Sophie
Jouvion, Grégory
Fevre, Cindy
Gessain, Grégoire
Thouvenot, Pierre
Eberl, Gérard
Di Santo, James P.
Peduto, Lucie
Lecuit, Marc
author_facet Disson, Olivier
Blériot, Camille
Jacob, Jean-Marie
Serafini, Nicolas
Dulauroy, Sophie
Jouvion, Grégory
Fevre, Cindy
Gessain, Grégoire
Thouvenot, Pierre
Eberl, Gérard
Di Santo, James P.
Peduto, Lucie
Lecuit, Marc
author_sort Disson, Olivier
collection PubMed
description 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.
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spelling pubmed-62197332019-05-05 Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion Disson, Olivier Blériot, Camille Jacob, Jean-Marie Serafini, Nicolas Dulauroy, Sophie Jouvion, Grégory Fevre, Cindy Gessain, Grégoire Thouvenot, Pierre Eberl, Gérard Di Santo, James P. Peduto, Lucie Lecuit, Marc J Exp Med Research Articles 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. Rockefeller University Press 2018-11-05 /pmc/articles/PMC6219733/ /pubmed/30355616 http://dx.doi.org/10.1084/jem.20181210 Text en © 2018 Disson et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Research Articles
Disson, Olivier
Blériot, Camille
Jacob, Jean-Marie
Serafini, Nicolas
Dulauroy, Sophie
Jouvion, Grégory
Fevre, Cindy
Gessain, Grégoire
Thouvenot, Pierre
Eberl, Gérard
Di Santo, James P.
Peduto, Lucie
Lecuit, Marc
Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title_full Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title_fullStr Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title_full_unstemmed Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title_short Peyer’s patch myeloid cells infection by Listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
title_sort peyer’s patch myeloid cells infection by listeria signals through gp38(+) stromal cells and locks intestinal villus invasion
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219733/
https://www.ncbi.nlm.nih.gov/pubmed/30355616
http://dx.doi.org/10.1084/jem.20181210
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