[Effects of interleukin-13 on the gob-5 and MUC5AC expression in lungs of a murine asthmatic model]

Zhonghua Jie He He Hu Xi Za Zhi. 2004 Dec;27(12):837-340.
[Article in Chinese]

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).

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.

MeSH terms

  • Animals
  • Asthma / metabolism*
  • Asthma / pathology
  • Chloride Channels / biosynthesis
  • Chloride Channels / genetics
  • Chloride Channels / metabolism*
  • Disease Models, Animal
  • Immunohistochemistry
  • Interleukin-13 / pharmacology*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mucin 5AC
  • Mucins / biosynthesis*
  • Mucins / genetics
  • Mucoproteins / biosynthesis*
  • Mucoproteins / genetics
  • Mucus / metabolism
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / genetics
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Chloride Channels
  • Clca3a1 protein, mouse
  • Interleukin-13
  • Muc5ac protein, mouse
  • Mucin 5AC
  • Mucins
  • Mucoproteins
  • RNA, Messenger