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dc.contributor.authorLiang, Minrui
dc.contributor.authorWang, Jiucun
dc.contributor.authorChu, Haiyan
dc.contributor.authorZhu, Xiaoxia
dc.contributor.authorHe, Hang
dc.contributor.authorLiu, Qiong
dc.contributor.authorQiu, Jianhua
dc.contributor.authorZhou, Xiaodong
dc.contributor.authorGuan, Ming
dc.contributor.authorXue, Yu
dc.contributor.authorChen, Xiangjun
dc.contributor.authorZou, Hejian
dc.date.accessioned2013-05-07T18:29:21Z
dc.date.issued2013
dc.identifier.citationLiang, 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.en_US
dc.identifier.issn0962-9351en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10611795
dc.description.abstractPulmonary 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.en_US
dc.language.isoen_USen_US
dc.publisherHindawi Publishing Corporationen_US
dc.relation.isversionofdoi:10.1155/2013/209179en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3588191/pdf/en_US
dash.licenseLAA
dc.titleInterleukin-22 Inhibits Bleomycin-Induced Pulmonary Fibrosisen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalMediators of Inflammationen_US
dash.depositing.authorQiu, Jianhua
dc.date.available2013-05-07T18:29:21Z
dc.identifier.doi10.1155/2013/209179*
dash.authorsorderedfalse
dash.contributor.affiliatedQiu, Jianhua


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