title: [Effect of dexamethasone on the expression of aquaporin-5 in the lungs of mice with acute allergic asthma].
abstract: OBJECTIVE
  To detect the expression of lung aquaporin 5 (AQP5) in mice with acute allergic asthma and the effect of dexamethasone (DEX) treatment on AQP5 expression, and investigate the role of AOP5 in asthma pathogenesis.
  
  
  METHODS
  Mouse models of acute allergic asthma were randomly divided into acute asthma group, normal control group and DEX treatment group. The total number of white blood cells, the subpopulations, and the levels of IL-5 and IFN-gamma were detected in the bronchoalveolar larvage fluid (BALF). The lung tissue AQP5 mRNA expression was detected by RT-PCR, and AQP5 distribution by immunohistochemical method.
  
  
  RESULTS
  In asthma group, the total white blood cells, eosinophils and IL-5 levels were all significantly higher (P<0.01) and IFN-gamma levels lower than those of the control group (P<0.01). After DEX treatment, the levels underwent a significant reverse change (P<0.05, P<0.01, P<0.01, and P<0.01, respectively). AQP5 mRNA expression in the asthma group was significantly higher than that in the control group (P<0.01), and was significantly lowered with DEX treatment (P<0.01). Extensive inflammatory changes, mucus hypersecrection, several edema and inflammatory cell infitration around the blood vessels were observed in the lung tissue of the mice in the asthma group. The morphological changes of the treatment group were significantly ameliorated. AQP5 protein was detected in the type I alveolar epithelial cells, the airway columnar epithelial cells and the apical membranes of the submucosal gland acinar cells in the control group. Stronger AQP5 protein expression was found in the asthma group.
  
  
  CONCLUSIONS
  AQP5 is over-expressed in mice with acute asthma which is possibly associated with mucus hypersecrection. DEX can inhibit AQP5 expression and ameliorate allergic airway inflammation, edema and mucus hypersecrection.
authors.affiliation: Department of Prediactrics, Second Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. w_b_jing@163.com
authors.forename: Bao-jing
authors.initials: BJ
authors.lastname: Wu
authors.forename: Jun
authors.initials: J
authors.lastname: Zhu
authors.forename: Wei-ping
authors.initials: WP
authors.lastname: Tan
authors.forename: Xian-di
authors.initials: XD
authors.lastname: Mai
authors.forename: Hua-rong
authors.initials: HR
authors.lastname: Huang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Wen-yi
authors.initials: WY
authors.lastname: Li
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D051402:Aquaporin 5 / Q000096:biosynthesis* / Q000235:genetics; D001249:Asthma / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D007150:Immunohistochemistry; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000893:Anti-Inflammatory Agents; D051402:Aquaporin 5; D012333:RNA, Messenger; D003907:Dexamethasone