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Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway

Listeria monocytogenes, as a model organism, is a causative agent of enteric pathogen that causes systemic infection. However, the interaction of L. monocytogenes and small intestinal epithelium has not been fully elucidated yet. In this study, mice and intestinal organoids were chosen as the models...

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Autores principales: Zhou, Cong, Zhang, Yuanyuan, Bassey, Anthony, Huang, Jie, Zou, Yafang, Ye, Keping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8990097/
https://www.ncbi.nlm.nih.gov/pubmed/35402308
http://dx.doi.org/10.3389/fcimb.2022.793335
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author Zhou, Cong
Zhang, Yuanyuan
Bassey, Anthony
Huang, Jie
Zou, Yafang
Ye, Keping
author_facet Zhou, Cong
Zhang, Yuanyuan
Bassey, Anthony
Huang, Jie
Zou, Yafang
Ye, Keping
author_sort Zhou, Cong
collection PubMed
description Listeria monocytogenes, as a model organism, is a causative agent of enteric pathogen that causes systemic infection. However, the interaction of L. monocytogenes and small intestinal epithelium has not been fully elucidated yet. In this study, mice and intestinal organoids were chosen as the models to investigate the influence of L. monocytogenes infection on the intestinal secretory cells and its differentiation-related pathways. Results confirmed the phenomenon of intestinal damage that L. monocytogenes infection could lead to villi damage in mice, which was accompanied by the increase of TNF-α production in jejunum as well as lipopolysaccharide (LPS) secretion in serum. Moreover, it was demonstrated that L. monocytogenes infection increased the number of goblet and Paneth cells in mice and intestinal organoids and upregulated the expression of Muc2 and Lyz. Furthermore, L. monocytogenes decreased the relative expression of Notch pathway-related genes (Jag1, Dll4, Notch1, and Hes1) while upregulating the relative expression of Math1 gene in mice and intestinal organoids. This indicated that L. monocytogenes infection caused the inhibition of Notch pathway, which may be the reason for the increased number of goblet and Paneth cells in the intestine. Collectively, these results are expected to provide more information on the mechanism of L. monocytogenes infection in the intestine.
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spelling pubmed-89900972022-04-09 Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway Zhou, Cong Zhang, Yuanyuan Bassey, Anthony Huang, Jie Zou, Yafang Ye, Keping Front Cell Infect Microbiol Cellular and Infection Microbiology Listeria monocytogenes, as a model organism, is a causative agent of enteric pathogen that causes systemic infection. However, the interaction of L. monocytogenes and small intestinal epithelium has not been fully elucidated yet. In this study, mice and intestinal organoids were chosen as the models to investigate the influence of L. monocytogenes infection on the intestinal secretory cells and its differentiation-related pathways. Results confirmed the phenomenon of intestinal damage that L. monocytogenes infection could lead to villi damage in mice, which was accompanied by the increase of TNF-α production in jejunum as well as lipopolysaccharide (LPS) secretion in serum. Moreover, it was demonstrated that L. monocytogenes infection increased the number of goblet and Paneth cells in mice and intestinal organoids and upregulated the expression of Muc2 and Lyz. Furthermore, L. monocytogenes decreased the relative expression of Notch pathway-related genes (Jag1, Dll4, Notch1, and Hes1) while upregulating the relative expression of Math1 gene in mice and intestinal organoids. This indicated that L. monocytogenes infection caused the inhibition of Notch pathway, which may be the reason for the increased number of goblet and Paneth cells in the intestine. Collectively, these results are expected to provide more information on the mechanism of L. monocytogenes infection in the intestine. Frontiers Media S.A. 2022-03-25 /pmc/articles/PMC8990097/ /pubmed/35402308 http://dx.doi.org/10.3389/fcimb.2022.793335 Text en Copyright © 2022 Zhou, Zhang, Bassey, Huang, Zou and Ye https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
Zhou, Cong
Zhang, Yuanyuan
Bassey, Anthony
Huang, Jie
Zou, Yafang
Ye, Keping
Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title_full Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title_fullStr Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title_full_unstemmed Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title_short Expansion of Intestinal Secretory Cell Population Induced by Listeria monocytogenes Infection: Accompanied With the Inhibition of NOTCH Pathway
title_sort expansion of intestinal secretory cell population induced by listeria monocytogenes infection: accompanied with the inhibition of notch pathway
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8990097/
https://www.ncbi.nlm.nih.gov/pubmed/35402308
http://dx.doi.org/10.3389/fcimb.2022.793335
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