Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis

DSpace/Manakin Repository

Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis

Citable link to this page

 

 
Title: Interleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosis
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

Note: Order does not necessarily reflect citation order of authors.

Citation: Liang, Minrui, Jiucun Wang, Haiyan Chu, Xiaoxia Zhu, Hang He, Qiong Liu, Jianhua Qiu, et al. 2013. Interleukin-22 inhibits bleomycin-induced pulmonary fibrosis. Mediators of Inflammation 2013:209179.
Full Text & Related Files:
Abstract: 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.
Published Version: doi:10.1155/2013/209179
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588191/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10611795
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters