title: Anti-interleukin-17 antibodies attenuate airway inflammation in tobacco-smoke-exposed mice.
abstract: BACKGROUND
  Our previous study showed that the interleukin-17 (IL-17) concentration in lung tissue and in bronchoalveolar lavage fluid (BALF) of rats with tobacco-smoke-induced chronic obstructive pulmonary disease (COPD) was higher than that of control group. However, whether IL-17 inhibitor could decrease the effect of tobacco smoking is not known yet.
  
  
  OBJECTIVE
  To investigate the significance of IL-17 antibodies (Ab) in tobacco-smoke-exposed (TSE) mice.
  
  
  METHODS
  Male C57/BL6 mice were randomly divided into three groups: TSE group, TSE + anti-IL-17 Ab group, and control group. The number of cells in BALF and the concentrations of IL-17, IL-6, IL-8 and MUC5AC in BALF and lung tissue homogenate were measured. Pulmonary function was measured by pressure sensors, and histologic analysis of the lungs was done in each group.
  
  
  RESULTS
  Lung function tests in TSE + anti-IL-17 Ab group were the same compared with TSE group (P > 0.05). The total cell count and the number of neutrophil cells in BALF were significantly higher in TSE group than the normal control group (P < 0.01). Compared with the TSE group, the total cell count in TSE + anti-IL-17 Ab group was decreased, and the percentage of neutrophils in BALF was highly decreased (P < 0.01). Airway inflammation was alleviated in TSE + anti-IL-17 Ab group by histologic analysis. The concentrations of IL-17 in lung tissue were significantly lower in TSE + anti-IL-17 Ab group than in TSE group (P < 0.01). IL-17 was mainly expressed in the epithelial cells in the airways of TSE mice. The concentration of IL-6, IL-8 and MUC5AC in BALF was decreased in TSE + anti-IL-17 Ab group compared with TSE group.
  
  
  CONCLUSIONS
  These data support a potential role for IL-17 in airway neutrophilic inflammation in TSE mice. Anti-IL-17 decreased the number of neutrophils as well as the concentration of MUC5AC in the BALF and attenuated neutrophilic airway inflammation.
authors: Department of Respiratory Medicine, Peking University Third Hospital, Beijing, China.
authors: Ning
authors: N
authors: Shen
authors: Jing
authors: J
authors: Wang
authors: Mingwu
authors: M
authors: Zhao
authors: Fei
authors: F
authors: Pei
authors: Bei
authors: B
authors: He
mesh_terms: D000818:Animals; D000906:Antibodies / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid; D007249:Inflammation; D019570:Inhalation Exposure; D020381:Interleukin-17 / Q000276:immunology / Q000378:metabolism*; D015850:Interleukin-6 / Q000097:blood / Q000378:metabolism; D016209:Interleukin-8 / Q000097:blood / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000503:physiopathology; D008171:Lung Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012906:Smoke / Q000009:adverse effects*; D014026:Nicotiana
chemical_list: D000906:Antibodies; D020381:Interleukin-17; D015850:Interleukin-6; D016209:Interleukin-8; D012906:Smoke