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Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β
Epithelial–mesenchymal transition (EMT) is an important mechanism of lung tissue repair after injury, but excessive EMT may lead to pulmonary fibrosis, respiratory failure, and even death. The EMT triggered by influenza A virus (IAV) and influenza B virus (IBV) is not well understood. We hypothesize...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8914340/ https://www.ncbi.nlm.nih.gov/pubmed/35283846 http://dx.doi.org/10.3389/fmicb.2022.841462 |
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author | Yang, Wenxian Bai, Xiaoyuan Li, Heqiao Li, Huizi Fan, Wenhui Zhang, He Liu, Wenjun Sun, Lei |
author_facet | Yang, Wenxian Bai, Xiaoyuan Li, Heqiao Li, Huizi Fan, Wenhui Zhang, He Liu, Wenjun Sun, Lei |
author_sort | Yang, Wenxian |
collection | PubMed |
description | Epithelial–mesenchymal transition (EMT) is an important mechanism of lung tissue repair after injury, but excessive EMT may lead to pulmonary fibrosis, respiratory failure, and even death. The EMT triggered by influenza A virus (IAV) and influenza B virus (IBV) is not well understood. We hypothesized that there was difference in EMT induced by different influenza virus strains. Here we discovered that both IAV [A/WSN/1933 (H1N1), WSN] and IBV (B/Yamagata/16/88, Yamagata) infection caused EMT in mouse lung and A549 cells, and more EMT-related genes were detected in mice and cells infected with WSN than those infected with Yamagata. Neuraminidase (NA) of IAV is able to activate latent TGF-β and the downstream TGF-β signaling pathway, which play a vital role in EMT. We observed that IAV (WSN) triggered more activated TGF-β expression and stronger TGF-β/smad2 signaling pathway than IBV (Yamagata). Most importantly, WSN NA combined more latent TGF-β than Yamagata NA in A549 cells. Collectively, these data demonstrate that both IAV and IBV induce TGF-β/smad2 signaling pathway to promote EMT, which might depend on the binding ability of NA to latent TGF-β. |
format | Online Article Text |
id | pubmed-8914340 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-89143402022-03-12 Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β Yang, Wenxian Bai, Xiaoyuan Li, Heqiao Li, Huizi Fan, Wenhui Zhang, He Liu, Wenjun Sun, Lei Front Microbiol Microbiology Epithelial–mesenchymal transition (EMT) is an important mechanism of lung tissue repair after injury, but excessive EMT may lead to pulmonary fibrosis, respiratory failure, and even death. The EMT triggered by influenza A virus (IAV) and influenza B virus (IBV) is not well understood. We hypothesized that there was difference in EMT induced by different influenza virus strains. Here we discovered that both IAV [A/WSN/1933 (H1N1), WSN] and IBV (B/Yamagata/16/88, Yamagata) infection caused EMT in mouse lung and A549 cells, and more EMT-related genes were detected in mice and cells infected with WSN than those infected with Yamagata. Neuraminidase (NA) of IAV is able to activate latent TGF-β and the downstream TGF-β signaling pathway, which play a vital role in EMT. We observed that IAV (WSN) triggered more activated TGF-β expression and stronger TGF-β/smad2 signaling pathway than IBV (Yamagata). Most importantly, WSN NA combined more latent TGF-β than Yamagata NA in A549 cells. Collectively, these data demonstrate that both IAV and IBV induce TGF-β/smad2 signaling pathway to promote EMT, which might depend on the binding ability of NA to latent TGF-β. Frontiers Media S.A. 2022-02-25 /pmc/articles/PMC8914340/ /pubmed/35283846 http://dx.doi.org/10.3389/fmicb.2022.841462 Text en Copyright © 2022 Yang, Bai, Li, Li, Fan, Zhang, Liu and Sun. 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 | Microbiology Yang, Wenxian Bai, Xiaoyuan Li, Heqiao Li, Huizi Fan, Wenhui Zhang, He Liu, Wenjun Sun, Lei Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title | Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title_full | Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title_fullStr | Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title_full_unstemmed | Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title_short | Influenza A and B Virus-Triggered Epithelial–Mesenchymal Transition Is Relevant to the Binding Ability of NA to Latent TGF-β |
title_sort | influenza a and b virus-triggered epithelial–mesenchymal transition is relevant to the binding ability of na to latent tgf-β |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8914340/ https://www.ncbi.nlm.nih.gov/pubmed/35283846 http://dx.doi.org/10.3389/fmicb.2022.841462 |
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