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
Waseda, Koichi Kaken ID
Taniguchi, Akihiko Kaken ID
Ikeda, Genyo
Nishimori, Hisakazu Kaken ID researchmap
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 Science KeyUT