title: IL-17A is essential to the development of elastase-induced pulmonary inflammation and emphysema in mice.
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.
authors: Department of Hematology, Oncology, Allergy and Respiratory Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan.
authors: Etsuko
authors: E
authors: Kurimoto
authors: Nobuaki
authors: N
authors: Miyahara
authors: Arihiko
authors: A
authors: Kanehiro
authors: Koichi
authors: K
authors: Waseda
authors: Akihiko
authors: A
authors: Taniguchi
authors: Genyo
authors: G
authors: Ikeda
authors: Hikari
authors: H
authors: Koga
authors: Hisakazu
authors: H
authors: Nishimori
authors: Yasushi
authors: Y
authors: Tanimoto
authors: Mikio
authors: M
authors: Kataoka
authors: Yoichiro
authors: Y
authors: Iwakura
authors: Erwin W
authors: EW
authors: Gelfand
authors: Mitsune
authors: M
authors: Tanimoto
mesh_terms: D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D018925:Chemokines / Q000378:metabolism; D005260:Female; D018836:Inflammation Mediators / Q000378:metabolism*; D020381:Interleukin-17 / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D008168:Lung / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D008170:Lung Compliance; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009504:Neutrophils / Q000276:immunology; D010196:Pancreatic Elastase; D011014:Pneumonia / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D011656:Pulmonary Emphysema / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D058504:Th17 Cells / Q000276:immunology; D013997:Time Factors
chemical_list: D018925:Chemokines; C098680:Il17a protein, mouse; D018836:Inflammation Mediators; D020381:Interleukin-17; D010196:Pancreatic Elastase