TY - JOUR
T1 - IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice
AU - Kurimoto, Etsuko
AU - Miyahara, Nobuaki
AU - Kanehiro, Arihiko
AU - Waseda, Koichi
AU - Taniguchi, Akihiko
AU - Ikeda, Genyo
AU - Koga, Hikari
AU - Nishimori, Hisakazu
AU - Tanimoto, Yasushi
AU - Kataoka, Mikio
AU - Iwakura, Yoichiro
AU - Gelfand, Erwin W.
AU - Tanimoto, Mitsune
PY - 2013/1/20
Y1 - 2013/1/20
N2 - 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.
AB - 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.
KW - Chronic obstructive pulmonary disease
KW - Elastase
KW - Emphysema
KW - IL-17
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U2 - 10.1186/1465-9921-14-5
DO - 10.1186/1465-9921-14-5
M3 - Article
C2 - 23331548
AN - SCOPUS:84872360544
VL - 14
JO - Respiratory Research
JF - Respiratory Research
SN - 1465-9921
IS - 1
M1 - 5
ER -