[Effects of interleukin-13 on the gob-5 and MUC5AC expression in lungs of a murine asthmatic model]
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Published on: July 7, 2017
Jian-Bo Liu1, Zhen-Xiang Zhang, Yong-Jian Xu
1Respiratory Disease Laboratory, Affiliated to Tongji Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
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).
Conclusion:
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.
