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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...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Rockefeller University Press
2018
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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. |
format | Online Article Text |
id | pubmed-6219733 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Rockefeller University Press |
record_format | MEDLINE/PubMed |
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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