title: Interleukin-22 inhibits bleomycin-induced pulmonary fibrosis.
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 γδ T 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.
authors.affiliation: Division of Rheumatology, Huashan Hospital, Fudan University, 12 Wulumuqi Zhong Road, Shanghai 200040, China.
authors.forename: Minrui
authors.initials: M
authors.lastname: Liang
authors.forename: Jiucun
authors.initials: J
authors.lastname: Wang
authors.forename: Haiyan
authors.initials: H
authors.lastname: Chu
authors.forename: Xiaoxia
authors.initials: X
authors.lastname: Zhu
authors.forename: Hang
authors.initials: H
authors.lastname: He
authors.forename: Qiong
authors.initials: Q
authors.lastname: Liu
authors.forename: Jianhua
authors.initials: J
authors.lastname: Qiu
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Zhou
authors.forename: Ming
authors.initials: M
authors.lastname: Guan
authors.forename: Yu
authors.initials: Y
authors.lastname: Xue
authors.forename: Xiangjun
authors.initials: X
authors.lastname: Chen
authors.forename: Hejian
authors.initials: H
authors.lastname: Zou
mesh_terms: D000818:Animals; D001761:Bleomycin / Q000009:adverse effects*; D015153:Blotting, Western; D002460:Cell Line; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D005434:Flow Cytometry; D006801:Humans; D007378:Interleukins / Q000378:metabolism* / Q000627:therapeutic use*; D051379:Mice; D008810:Mice, Inbred C57BL; D011658:Pulmonary Fibrosis / Q000139:chemically induced* / Q000188:drug therapy* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000097043:Interleukin-22
chemical_list: D001761:Bleomycin; D007378:Interleukins; D000097043:Interleukin-22