title: [Roles of Th17 lymphocytes and  inflammatory cytokines in airway inflammation exacerbation of murine asthmatic model].
abstract: OBJECTIVE
  To investigate the roles of Th17 lymphocytes and its inflammatory cytokines in airway inflammation exacerbation of murine asthmatic model.
  
  
  METHODS
  Twenty mice were randomized into control group and asthma group. For the murine asthma model,  the mice were sensitized and challenged with ovalbumin (OVA). The control mice were given normal  saline alone under the same conditions as the asthma group. We observed the changes in cellular proportions in the bronchoalveolar lavage fluid (BALF) under a light microscope and the histological changes in lung tissue by HE staining. The levels of IL-4,  IFN-γ and IL-17 were detected by ELISA. Th1,  Th2 and Th17 cells in the peripheral blood were detected by flow cytometry. We did a correlation analysis between Th1,  Th2 and Th17 cells in the peripheral blood and neutrophils in BALF.
  
  
  RESULTS
  The total cell number and the percentages of neutrophils,  eosinophils and lymphocytes in BALF of the asthmatic mice were significantly higher than those in the control mice (P<0.05). The neutrophils and eosinophils infiltration in pulmonary tissue was also dramatically detected in asthmatic mice. The levels of IL-4 and IL-17 were significantly higher than those in the control mice (P<0.05),  while the level of IFN-γ was much lower than in the control mice (P<0.05). Besides,  the percentages of Th2 and Th17 cells in peripheral blood were significantly higher in the asthmatic mice than in the control mice (P<0.05). The expression of Th17 was positively correlated with the levels of neutrophils in BALF(r(Th17);=0.394,  P<0.05),  and the expression of Th1 was negatively correlated with the level of neutrophils in BALF (r(Th1);=-0.446,  P<0.05).
  
  
  CONCLUSIONS
  Th17 cells could induce the recruitment of inflammatory cytokines and neutrophils into airways,  which might aggravate the asthmatic inflammation and be related with asthma exacerbation.
authors.affiliation: Department of Respiratory Diseases, Qianfoshan Hospital, Shandong University, Jinan, China. lihongjiastar@163.com
authors.forename: Hong-jia
authors.initials: HJ
authors.lastname: Li
authors.forename: Cai-qing
authors.initials: CQ
authors.lastname: Zhang
authors.forename: Cui-xiang
authors.initials: CX
authors.lastname: Yu
authors.forename: Fen
authors.initials: F
authors.lastname: Liu
authors.forename: Qing-ling
authors.initials: QL
authors.lastname: Gai
authors.forename: Jin-xiang
authors.initials: JX
authors.lastname: Wu
authors.forename: Ji-ping
authors.initials: JP
authors.lastname: Zhao
authors.forename: Liang
authors.initials: L
authors.lastname: Dong
mesh_terms: D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D016207:Cytokines / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D008168:Lung / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D058504:Th17 Cells / Q000502:physiology*
chemical_list: D016207:Cytokines