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IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice

Etsuko Kurimoto1, Nobuaki Miyahara1*, Arihiko Kanehiro1, Koichi Waseda1, Akihiko Taniguchi1, Genyo Ikeda1, Hikari Koga1, Hisakazu Nishimori1, Yasushi Tanimoto1, Mikio Kataoka1, Yoichiro Iwakura2, Erwin W Gelfand3 and Mitsune Tanimoto1

Author Affiliations

1 Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan

2 Center for Experimental Medicine and Systems Biology, Institute of Medical Science, University of Tokyo, Tokyo, Japan

3 Division of Cell Biology, Department of Pediatrics, National Jewish Health, Denver, CO, USA

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Respiratory Research 2013, 14:5  doi:10.1186/1465-9921-14-5

Published: 20 January 2013

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