title: [Effects of interleukin-13 on the gob-5 and MUC5AC expression in lungs of a murine asthmatic model].
abstract: OBJECTIVE
  To study the influence of interleukin-13 (IL-13) on the gob-5, a member of Ca(2+)-activated Cl(-) channel and mucin gene MUC5AC expression in lungs of a murine asthmatic model, and to investigate their effects on the pathogenesis of asthma.
  
  
  METHODS
  Forty-five male BALB/c mice were randomly divided into a control group, an asthmatic group and an IL-13 group. Expression of gob-5 mRNA, MUC5AC mRNA and MUC5AC protein in the lungs were detected by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical assay respectively.
  
  
  RESULTS
  No gob-5 mRNA expression in the lung was detected in the control group, while it was positive in the asthmatic group. The gob-5 mRNA in the lung of the IL-13 group and the asthmatic group was 1.246 +/- 0.008 and 1.136 +/- 0.007 respectively (P < 0.01). In the asthmatic group, both MUC5AC mRNA (0.161 +/- 0.011) and protein expression (7 mice positive) increased compared with the control group (0.070 +/- 0.004 and 2 mice positive, respectively) (P < 0.01 and 0.05, respectively). IL-13 increased the expression of MUC5AC mRNA (0.250 +/- 0.014) and protein (13 mice positive) in the lung of the asthmatic group, and there was a significant difference between the IL-13 group and either the control group (0.070 +/- 0.004 and 2 mice positive, respectively) or the asthmatic group (0.161 +/- 0.011 and 7 mice positive, respectively, all P < 0.05). There was a significant association between gob-5 mRNA expression and MUC5AC mRNA expression in both the IL-13 group and the asthmatic group (r = 0.986 and 0.961, respectively, both P < 0.05).
  
  
  CONCLUSIONS
  IL-13 is a critical cytokine in the pathogenesis of asthma, and gob-5 may be one of the important genes in inducing airway mucus overproduction of asthma.
authors.affiliation: Respiratory Disease Laboratory, Affiliated to Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
authors.forename: Jian-Bo
authors.initials: JB
authors.lastname: Liu
authors.forename: Zhen-Xiang
authors.initials: ZX
authors.lastname: Zhang
authors.forename: Yong-Jian
authors.initials: YJ
authors.lastname: Xu
authors.forename: Li-Hua
authors.initials: LH
authors.lastname: Xing
authors.forename: Hui-Lan
authors.initials: HL
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001249:Asthma / Q000378:metabolism* / Q000473:pathology; D018118:Chloride Channels / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism*; D004195:Disease Models, Animal; D007150:Immunohistochemistry; D018793:Interleukin-13 / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D055271:Mucin 5AC; D009077:Mucins / Q000096:biosynthesis* / Q000235:genetics; D009088:Mucoproteins / Q000096:biosynthesis* / Q000235:genetics; D009093:Mucus / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D018118:Chloride Channels; C116464:Clca3a1 protein, mouse; D018793:Interleukin-13; C524679:Muc5ac protein, mouse; D055271:Mucin 5AC; D009077:Mucins; D009088:Mucoproteins; D012333:RNA, Messenger