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A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells
Respiratory syncytial virus (RSV) is the major cause of bronchitis, asthma, and severe lower respiratory tract disease in infants and young children. The airway epithelium, which has a well-developed barrier regulated by tight junctions, is the first line of defense during respiratory virus infectio...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128518/ https://www.ncbi.nlm.nih.gov/pubmed/21562222 http://dx.doi.org/10.1091/mbc.E10-11-0875 |
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author | Masaki, Tomoyuki Kojima, Takashi Okabayashi, Tamaki Ogasawara, Noriko Ohkuni, Tsuyoshi Obata, Kazufumi Takasawa, Akira Murata, Masaki Tanaka, Satoshi Hirakawa, Satoshi Fuchimoto, Jun Ninomiya, Takafumi Fujii, Nobuhiro Tsutsumi, Hiroyuki Himi, Tetsuo Sawada, Norimasa |
author_facet | Masaki, Tomoyuki Kojima, Takashi Okabayashi, Tamaki Ogasawara, Noriko Ohkuni, Tsuyoshi Obata, Kazufumi Takasawa, Akira Murata, Masaki Tanaka, Satoshi Hirakawa, Satoshi Fuchimoto, Jun Ninomiya, Takafumi Fujii, Nobuhiro Tsutsumi, Hiroyuki Himi, Tetsuo Sawada, Norimasa |
author_sort | Masaki, Tomoyuki |
collection | PubMed |
description | Respiratory syncytial virus (RSV) is the major cause of bronchitis, asthma, and severe lower respiratory tract disease in infants and young children. The airway epithelium, which has a well-developed barrier regulated by tight junctions, is the first line of defense during respiratory virus infection. In upper airway human nasal epithelial cells (HNECs), however, the primary site of RSV infection, the mechanisms of replication and budding of RSV, and the epithelial cell responses, including the tight junctional barrier, remain unknown. To investigate the detailed mechanisms of replication and budding of RSV in HNECs and the epithelial cell responses, we established an RSV-infected model using human telomerase reverse transcriptase–-transfected HNECs. We first found that the expression and barrier function of tight junction molecules claudin-4 and occludin were markedly induced together with production of proinflammatory cytokines interleukin 8 and tumor necrosis factor-α in HNECs after RSV infection, and the induction of tight junction molecules possibly contributed to budding of RSV. Furthermore, the replication and budding of RSV and the epithelial cell responses in HNECs were regulated via a protein kinase C δ/hypoxia-inducible factor-1α/nuclear factor-κB pathway. The control of this pathway in HNECs may be useful not only for prevention of replication and budding of RSV, but also in therapy for RSV-induced respiratory pathogenesis. |
format | Online Article Text |
id | pubmed-3128518 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-31285182011-09-16 A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells Masaki, Tomoyuki Kojima, Takashi Okabayashi, Tamaki Ogasawara, Noriko Ohkuni, Tsuyoshi Obata, Kazufumi Takasawa, Akira Murata, Masaki Tanaka, Satoshi Hirakawa, Satoshi Fuchimoto, Jun Ninomiya, Takafumi Fujii, Nobuhiro Tsutsumi, Hiroyuki Himi, Tetsuo Sawada, Norimasa Mol Biol Cell Articles Respiratory syncytial virus (RSV) is the major cause of bronchitis, asthma, and severe lower respiratory tract disease in infants and young children. The airway epithelium, which has a well-developed barrier regulated by tight junctions, is the first line of defense during respiratory virus infection. In upper airway human nasal epithelial cells (HNECs), however, the primary site of RSV infection, the mechanisms of replication and budding of RSV, and the epithelial cell responses, including the tight junctional barrier, remain unknown. To investigate the detailed mechanisms of replication and budding of RSV in HNECs and the epithelial cell responses, we established an RSV-infected model using human telomerase reverse transcriptase–-transfected HNECs. We first found that the expression and barrier function of tight junction molecules claudin-4 and occludin were markedly induced together with production of proinflammatory cytokines interleukin 8 and tumor necrosis factor-α in HNECs after RSV infection, and the induction of tight junction molecules possibly contributed to budding of RSV. Furthermore, the replication and budding of RSV and the epithelial cell responses in HNECs were regulated via a protein kinase C δ/hypoxia-inducible factor-1α/nuclear factor-κB pathway. The control of this pathway in HNECs may be useful not only for prevention of replication and budding of RSV, but also in therapy for RSV-induced respiratory pathogenesis. The American Society for Cell Biology 2011-07-01 /pmc/articles/PMC3128518/ /pubmed/21562222 http://dx.doi.org/10.1091/mbc.E10-11-0875 Text en © 2011 Masaki et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society of Cell Biology. |
spellingShingle | Articles Masaki, Tomoyuki Kojima, Takashi Okabayashi, Tamaki Ogasawara, Noriko Ohkuni, Tsuyoshi Obata, Kazufumi Takasawa, Akira Murata, Masaki Tanaka, Satoshi Hirakawa, Satoshi Fuchimoto, Jun Ninomiya, Takafumi Fujii, Nobuhiro Tsutsumi, Hiroyuki Himi, Tetsuo Sawada, Norimasa A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title | A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title_full | A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title_fullStr | A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title_full_unstemmed | A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title_short | A nuclear factor-κB signaling pathway via protein kinase C δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
title_sort | nuclear factor-κb signaling pathway via protein kinase c δ regulates replication of respiratory syncytial virus in polarized normal human nasal epithelial cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3128518/ https://www.ncbi.nlm.nih.gov/pubmed/21562222 http://dx.doi.org/10.1091/mbc.E10-11-0875 |
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