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.

journal_name

Mediators Inflamm

authors

Liang M,Wang J,Chu H,Zhu X,He H,Liu Q,Qiu J,Zhou X,Guan M,Xue Y,Chen X,Zou H

doi

10.1155/2013/209179

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

209179

eissn

0962-9351

issn

1466-1861

journal_volume

2013

pub_type

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