Identification of MUC5B mucin gene in human middle ear with chronic otitis media

被引:37
|
作者
Kawano, H
Paparella, MM
Ho, SB
Schachern, PA
Morizono, N
Le, CT
Lin, JZ
机构
[1] Univ Minnesota, Otopathol Mol Biol Lab, Otitis Med Res Ctr, Dept Otolaryngol, Minneapolis, MN USA
[2] Univ Minnesota, Sch Med, Div Biostat, Minneapolis, MN 55455 USA
[3] Univ Minnesota, Sch Publ Hlth, Vet Adm Med Ctr, Minneapolis, MN USA
[4] Minnesota Ear Head & Neck Clin, Minneapolis, MN 55454 USA
来源
LARYNGOSCOPE | 2000年 / 110卷 / 04期
关键词
D O I
10.1097/00005537-200004000-00024
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objectives: To identify the mucin gene and its expressing cells in the middle ear mucosa with chronic otitis media (COM), and to study the correlation between infiltration of inflammatory cells in the submucosa and expression of the mucin gene in the mucosal epithelium with COM Study Design: Middle ear mucosal specimens removed from the inferior promontory area of 19 patients undergoing middle ear surgery for COM were studied Methods: Sections were stained with H&E, Alcian blue-periodic acid Schiff (AB-PAS), polyclonal MUC5B antibody, and specific MUC5B riboprobe for histological, histochemical, immunohistochemical, and mucin mRNA analyses. Results: H&E staining revealed pseudostratified epithelia in 18 of the middle ear specimens with COM and cuboidal secretory epithelia in one. AB-PAS staining of epithelia revealed abundant secretory cells and their products (glycoconjugates). In situ hybridization and immunohistochemistry studies demonstrated that the secretory cells of the middle ear mucosa with COM expressed MUC5B mucin mRNA and its product MUC5B mucin. Conclusions: The MUC5B mucin gene and its product were identified in the middle ear secretory cells of patients with COM. Its expression was extensive in pseudostratified mucosal epithelia and related to infiltration of inflammatory cells in the submucosa of the middle ear cleft with COM, suggestive that inflammatory cell products are involved in the production of MUC5B.
引用
收藏
页码:668 / 673
页数:6
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