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Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis

Pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Recent insight has suggested that early injury/inflammation of alveolar epithelial cells could lead to dysregulation of tissue repair driven by multiple cytokines. Although dysregulation of interleukin...

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Autores principales: Liang, Minrui, Wang, Jiucun, Chu, Haiyan, Zhu, Xiaoxia, He, Hang, Liu, Qiong, Qiu, Jianhua, Zhou, Xiaodong, Guan, Ming, Xue, Yu, Chen, Xiangjun, Zou, Hejian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588191/
https://www.ncbi.nlm.nih.gov/pubmed/23476100
http://dx.doi.org/10.1155/2013/209179
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author Liang, Minrui
Wang, Jiucun
Chu, Haiyan
Zhu, Xiaoxia
He, Hang
Liu, Qiong
Qiu, Jianhua
Zhou, Xiaodong
Guan, Ming
Xue, Yu
Chen, Xiangjun
Zou, Hejian
author_facet Liang, Minrui
Wang, Jiucun
Chu, Haiyan
Zhu, Xiaoxia
He, Hang
Liu, Qiong
Qiu, Jianhua
Zhou, Xiaodong
Guan, Ming
Xue, Yu
Chen, Xiangjun
Zou, Hejian
author_sort Liang, Minrui
collection PubMed
description Pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Recent insight has suggested that early injury/inflammation of alveolar epithelial cells could lead to dysregulation of tissue repair driven by multiple cytokines. Although dysregulation of interleukin- (IL-) 22 is involved in various pulmonary pathophysiological processes, the role of IL-22 in fibrotic lung diseases is still unclear and needs to be further addressed. Here we investigated the effect of IL-22 on alveolar epithelial cells in the bleomycin- (BLM-) induced pulmonary fibrosis. BLM-treated mice showed significantly decreased level of IL-22 in the lung. IL-22 produced γ δT cells were also decreased significantly both in the tissues of lungs and spleens. Administration of recombinant human IL-22 to alveolar epithelial cell line A549 cells ameliorated epithelial to mesenchymal transition (EMT) and partially reversed the impaired cell viability induced by BLM. Furthermore, blockage of IL-22 deteriorated pulmonary fibrosis, with elevated EMT marker (α-smooth muscle actin (α-SMA)) and overactivated Smad2. Our results indicate that IL-22 may play a protective role in the development of BLM-induced pulmonary fibrosis and may suggest IL-22 as a novel immunotherapy tool in treating pulmonary fibrosis.
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spelling pubmed-35881912013-03-09 Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis Liang, Minrui Wang, Jiucun Chu, Haiyan Zhu, Xiaoxia He, Hang Liu, Qiong Qiu, Jianhua Zhou, Xiaodong Guan, Ming Xue, Yu Chen, Xiangjun Zou, Hejian Mediators Inflamm Research Article Pulmonary fibrosis is a progressive and fatal fibrotic disease of the lungs with unclear etiology. Recent insight has suggested that early injury/inflammation of alveolar epithelial cells could lead to dysregulation of tissue repair driven by multiple cytokines. Although dysregulation of interleukin- (IL-) 22 is involved in various pulmonary pathophysiological processes, the role of IL-22 in fibrotic lung diseases is still unclear and needs to be further addressed. Here we investigated the effect of IL-22 on alveolar epithelial cells in the bleomycin- (BLM-) induced pulmonary fibrosis. BLM-treated mice showed significantly decreased level of IL-22 in the lung. IL-22 produced γ δT cells were also decreased significantly both in the tissues of lungs and spleens. Administration of recombinant human IL-22 to alveolar epithelial cell line A549 cells ameliorated epithelial to mesenchymal transition (EMT) and partially reversed the impaired cell viability induced by BLM. Furthermore, blockage of IL-22 deteriorated pulmonary fibrosis, with elevated EMT marker (α-smooth muscle actin (α-SMA)) and overactivated Smad2. Our results indicate that IL-22 may play a protective role in the development of BLM-induced pulmonary fibrosis and may suggest IL-22 as a novel immunotherapy tool in treating pulmonary fibrosis. Hindawi Publishing Corporation 2013 2013-02-18 /pmc/articles/PMC3588191/ /pubmed/23476100 http://dx.doi.org/10.1155/2013/209179 Text en Copyright © 2013 Minrui Liang et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Liang, Minrui
Wang, Jiucun
Chu, Haiyan
Zhu, Xiaoxia
He, Hang
Liu, Qiong
Qiu, Jianhua
Zhou, Xiaodong
Guan, Ming
Xue, Yu
Chen, Xiangjun
Zou, Hejian
Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title_full Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title_fullStr Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title_full_unstemmed Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title_short Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
title_sort interleukin-22 inhibits bleomycin-induced pulmonary fibrosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588191/
https://www.ncbi.nlm.nih.gov/pubmed/23476100
http://dx.doi.org/10.1155/2013/209179
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