Korean J Otolaryngol-Head Neck Surg.
2001 Jun;44(6):600-605.
Expression and regulation of MUC8 & MUC5AC by various cytokines in normal human nasal epithelial cells
- Affiliations
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- 1Department of Otorhinolaryngology
- 2BK 21 Center for Medical Science, Yonsei University College of Medicine, Seoul, Korea. jhyoon@yumc.yonsei.ac.kr
- 3Department of Otorhinolaryngology National Health Insurance Corporation Ilsan Hospital, Koyang
- 4Department of Otolaryngology-Head & Neck Surgery College of Medicine, The Catholic University, Seoul, Korea.
Abstract
- BACKGROUND AND OBJECTIVES
Sinusitis is one of the most commonly reported diseases in the world. A network of inflammatory mediators is known to be involved in the pathogenesis of chronic sinusitis and nasal mucus secretion may also be under the control of an inflammatory mediator network. To date, 12 human mucin genes have been identified; however, the regulation of MUC8 has not yet been found out. In this study, we described the regulation of the MUC8 mRNA expression by inflammatory mediators and investigated its cellular location. MATERIALS AND METHOD: MUC8 mRNA and MUC5AC mRNA were detected in culture using passage-2 normal human nasal epithelial (NHNE) cells after the treatment with a mixture of following inflammatory mediators; TNF-alpha, IL-1beta, LPS, IL-4, PAF. The translocation of MUC8 mRNA from the nucleus to the cytoplasm was investigated by treating the inflammatory mediators with in situ hybridization.
RESULTS
We found that a mixture of inflammatory mediators increased the MUC8 mRNA expression but decreased the MUC5AC mRNA expression in cultured normal human nasal epithelial cells. Among the inflammatory mediators, Interleukin-4 was responsible for the decrease in the MUC5AC mRNA expression and the MUC5AC mucin secretion. We also found that MUC8 mRNA resides in the nucleus of goblet cells and is transported into the cytoplasm following the treatment with inflammatory mediators.
CONCLUSION
These results indicate that MUC8 may play an important role in the pathogenesis of mucus hypersecretion in chronic sinusitis.
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