このエントリーをはてなブックマークに追加
ID 52339
FullText URL
Author
Kurimoto, Etsuko
Ikeda, Genyo
Tanimoto, Yasushi
Iwakura, Yoichiro
Gelfand, Erwin W.
Abstract
Background: Pulmonary emphysema is characterized by alveolar destruction and persistent inflammation of the airways. Although IL-17A contributes to many chronic inflammatory diseases, it's role in the inflammatory response of elastase-induced emphysema remains unclear. Methods: In a model of elastase-induced pulmonary emphysema we examined the response of IL-17A-deficient mice, monitoring airway inflammation, static compliance, lung histology and levels of neutrophil-related chemokine and pro-inflammatory cytokines in bronchoalveolar lavage (BAL) fluid. Results: Wild-type mice developed emphysematous changes in the lung tissue on day 21 after elastase treatment, whereas emphysematous changes were decreased in IL-17A-deficient mice compared to wild-type mice. Neutrophilia in BAL fluid, seen in elastase-treated wild-type mice, was reduced in elastase-treated IL-17A-deficient mice on day 4, associated with decreased levels of KC, MIP-2 and IL-1 beta. Elastase-treated wild-type mice showed increased IL-17A levels as well as increased numbers of IL-17A+ CD4 T cells in the lung in the initial period following elastase treatment. Conclusions: These data identify the important contribution of IL-17A in the development of elastase-induced pulmonary inflammation and emphysema. Targeting IL-17A in emphysema may be a potential therapeutic strategy for delaying disease progression.
Keywords
IL-17
Elastase
Emphysema
Chronic obstructive pulmonary disease
Published Date
2013-01-20
Publication Title
Respiratory Research
Volume
volume14
Publisher
Biomed Central Ltd
ISSN
1465-993X
Content Type
Journal Article
language
英語
File Version
publisher
Refereed
True
DOI
Web of Sience KeyUT