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 interleuki...

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Main Authors: Minrui Liang, Jiucun Wang, Haiyan Chu, Xiaoxia Zhu, Hang He, Qiong Liu, Jianhua Qiu, Xiaodong Zhou, Ming Guan, Yu Xue, Xiangjun Chen, Hejian Zou
Format: Article
Language:English
Published: Wiley 2013-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2013/209179
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author Minrui Liang
Jiucun Wang
Haiyan Chu
Xiaoxia Zhu
Hang He
Qiong Liu
Jianhua Qiu
Xiaodong Zhou
Ming Guan
Yu Xue
Xiangjun Chen
Hejian Zou
author_facet Minrui Liang
Jiucun Wang
Haiyan Chu
Xiaoxia Zhu
Hang He
Qiong Liu
Jianhua Qiu
Xiaodong Zhou
Ming Guan
Yu Xue
Xiangjun Chen
Hejian Zou
author_sort Minrui Liang
collection DOAJ
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 γδT 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 doaj-art-32375ccaa42147dbba4bd27a3f4332ef2025-08-20T02:07:41ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/209179209179Interleukin-22 Inhibits Bleomycin-Induced Pulmonary FibrosisMinrui Liang0Jiucun Wang1Haiyan Chu2Xiaoxia Zhu3Hang He4Qiong Liu5Jianhua Qiu6Xiaodong Zhou7Ming Guan8Yu Xue9Xiangjun Chen10Hejian Zou11Division of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai 200040, ChinaInstitute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, ChinaInstitute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, ChinaDivision of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai 200040, ChinaDepartment of Pancreatic Surgery, Pancreatic Disease Institute, Huashan Hospital, Fudan University, Shanghai 200040, ChinaInstitute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, ChinaDepartment of Neurology and Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USADivision of Rheumatology and Clinical Immunogenetics, Department of Internal Medicine, The University of Texas Medical School, Houston, TX 77030, USAInstitute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, ChinaDivision of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai 200040, ChinaInstitute of Rheumatology, Immunology and Allergy, Fudan University, Shanghai 200040, ChinaDivision of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai 200040, ChinaPulmonary 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 γδT 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.http://dx.doi.org/10.1155/2013/209179
spellingShingle Minrui Liang
Jiucun Wang
Haiyan Chu
Xiaoxia Zhu
Hang He
Qiong Liu
Jianhua Qiu
Xiaodong Zhou
Ming Guan
Yu Xue
Xiangjun Chen
Hejian Zou
Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
Mediators of Inflammation
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
url http://dx.doi.org/10.1155/2013/209179
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AT hanghe interleukin22inhibitsbleomycininducedpulmonaryfibrosis
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