Korean J Otolaryngol-Head Neck Surg.  2000 Apr;43(4):377-382.

Mucin and Lysozyme Expression in the Epithelium of Normal Human Nasal Inferior Turbinate and Polyps

Affiliations
  • 1Department of Otorhinolaryngology-Head & Neck Surgery, College of Medicine, The Catholic University, Korea.
  • 2Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea.

Abstract

BACKGROUND AND OBJECTIVES: In chronic bronchitis, rhinitis or cystic fibrosis, the number of goblet cells increases along with hypertrophy of mucous cells in submucosal gland, resulting ineffective mucociliary clearance. But, it is still not fully understood what role each gene plays in producing airway secretions. This study aimed to figure out which mucin gene is expressed in the epithelium of normal human nasal mucosa and nasal polyps, and to verify whether the epithelium of nasal polyp itself contributes to the increased nasal secretion as in chronic sinusitis with nasal polyp.
MATERIALS AND METHODS
Normal nasal epithelial cells were obt assay. And, RT-PCR was used for the detection of mucin mRNA and lysozyme mRNA.
RESULTS
The level of intracellular mucin was 2.9 times higher in the epithelium of nasal polyp, and this was statistically significant. Among seven mucin genes (MUC1, 2, 4, 5AC, 5B, 7, 8) expressed in the epithelium of normal inferior turbinate and polyps, MUC2 and MUC8 were more strongly expressed in the epithelium of nasal polyp than those of normal inferior turbinate.
CONCLUSION
This results suggest that the polyp epithelium itself is contributing to increased secretion in chronic sinusitis, and MUC2 and MUC8 are thought tbe responsible for this change. However, further study is required to uncover the full sequence of MUC8 mRNA and its exact function.

Keyword

Mucin; Lysozyme; Mucin gene; Nasal epithelium; Polyp

MeSH Terms

Bronchitis, Chronic
Cystic Fibrosis
Epithelial Cells
Epithelium*
Goblet Cells
Humans*
Hypertrophy
Mucins*
Mucociliary Clearance
Muramidase*
Nasal Mucosa
Nasal Polyps
Polyps*
Rhinitis
RNA, Messenger
Sinusitis
Turbinates*
Mucins
Muramidase
RNA, Messenger
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