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ID 52339
フルテキストURL
著者
Kurimoto, Etsuko Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Miyahara, Nobuaki Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Kanehiro, Arihiko Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Waseda, Koichi Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Taniguchi, Akihiko Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Ikeda, Genyo Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Koga, Hikari Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Nishimori, Hisakazu Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Tanimoto, Yasushi Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Kataoka, Mikio Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
Iwakura, Yoichiro Univ Tokyo, Inst Med Sci, Ctr Expt Med & Syst Biol
Gelfand, Erwin W. Natl Jewish Hlth, Dept Pediat, Div Cell Biol
Tanimoto, Mitsune Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Hematol Oncol Allergy & Resp Med
抄録
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.
キーワード
IL-17
Elastase
Emphysema
Chronic obstructive pulmonary disease
発行日
2013-01-20
出版物タイトル
Respiratory Research
14巻
出版者
Biomed Central Ltd
ISSN
1465-993X
資料タイプ
学術雑誌論文
言語
English
OAI-PMH Set
岡山大学
論文のバージョン
publisher
査読
有り
DOI
Web of Sience KeyUT