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H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation
The barrier function of nasal mucosal epithelial cells plays an irreplaceable role in the spread and expansion of viruses in the body. This study found that influenza A virus H1N1 could induce apoptosis of nasal mucosal epithelial progenitor cells, cause an inflammatory response, and trigger the mat...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9095954/ https://www.ncbi.nlm.nih.gov/pubmed/35572503 http://dx.doi.org/10.3389/fimmu.2022.879575 |
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author | Zhu, Fangyuan Teng, Zhenxiao Zhou, Xuanchen Xu, Runtong Bing, Xin Shi, Lei Guo, Na Wang, Min Liu, Chengcheng Xia, Ming |
author_facet | Zhu, Fangyuan Teng, Zhenxiao Zhou, Xuanchen Xu, Runtong Bing, Xin Shi, Lei Guo, Na Wang, Min Liu, Chengcheng Xia, Ming |
author_sort | Zhu, Fangyuan |
collection | PubMed |
description | The barrier function of nasal mucosal epithelial cells plays an irreplaceable role in the spread and expansion of viruses in the body. This study found that influenza A virus H1N1 could induce apoptosis of nasal mucosal epithelial progenitor cells, cause an inflammatory response, and trigger the maturation and recruitment of nasal submucosal dendritic cells (DCs), but the mechanism remained unclear. Therefore, we used RNA sequencing and high-resolution untargeted metabolomics to sequence and perform combined bioinformatic analysis of H1N1 virus-infected nasal mucosal epithelial cells from 6 different patients. The abnormal arginine metabolism signaling pathway caused by H1N1 virus infection was screened out, and arginase inhibitors were used to interfere with the abnormal arginine metabolism and the maturation and recruitment of submucosal DCs caused by the H1N1 virus in vitro and in vivo. We conclude that H1N1 influenza virus promotes the recruitment and maturation of submucosal DCs by causing abnormal arginine metabolism in nasal mucosal epithelial cells, thereby triggering respiratory mucosal immunity. |
format | Online Article Text |
id | pubmed-9095954 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-90959542022-05-13 H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation Zhu, Fangyuan Teng, Zhenxiao Zhou, Xuanchen Xu, Runtong Bing, Xin Shi, Lei Guo, Na Wang, Min Liu, Chengcheng Xia, Ming Front Immunol Immunology The barrier function of nasal mucosal epithelial cells plays an irreplaceable role in the spread and expansion of viruses in the body. This study found that influenza A virus H1N1 could induce apoptosis of nasal mucosal epithelial progenitor cells, cause an inflammatory response, and trigger the maturation and recruitment of nasal submucosal dendritic cells (DCs), but the mechanism remained unclear. Therefore, we used RNA sequencing and high-resolution untargeted metabolomics to sequence and perform combined bioinformatic analysis of H1N1 virus-infected nasal mucosal epithelial cells from 6 different patients. The abnormal arginine metabolism signaling pathway caused by H1N1 virus infection was screened out, and arginase inhibitors were used to interfere with the abnormal arginine metabolism and the maturation and recruitment of submucosal DCs caused by the H1N1 virus in vitro and in vivo. We conclude that H1N1 influenza virus promotes the recruitment and maturation of submucosal DCs by causing abnormal arginine metabolism in nasal mucosal epithelial cells, thereby triggering respiratory mucosal immunity. Frontiers Media S.A. 2022-04-28 /pmc/articles/PMC9095954/ /pubmed/35572503 http://dx.doi.org/10.3389/fimmu.2022.879575 Text en Copyright © 2022 Zhu, Teng, Zhou, Xu, Bing, Shi, Guo, Wang, Liu and Xia 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 | Immunology Zhu, Fangyuan Teng, Zhenxiao Zhou, Xuanchen Xu, Runtong Bing, Xin Shi, Lei Guo, Na Wang, Min Liu, Chengcheng Xia, Ming H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title | H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title_full | H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title_fullStr | H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title_full_unstemmed | H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title_short | H1N1 Influenza Virus-Infected Nasal Mucosal Epithelial Progenitor Cells Promote Dendritic Cell Recruitment and Maturation |
title_sort | h1n1 influenza virus-infected nasal mucosal epithelial progenitor cells promote dendritic cell recruitment and maturation |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9095954/ https://www.ncbi.nlm.nih.gov/pubmed/35572503 http://dx.doi.org/10.3389/fimmu.2022.879575 |
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