Effect of Tumor Necrosis Factor-alpha on Experimental Otitis Media with Effusion.
- Author:
Dong Hee LEE
1
;
Yong Soo PARK
;
Young Chul CHOI
;
Eun Ju JEON
;
Sang Won YEO
Author Information
1. Department of Otolaryngology-HNS, College of Medicine, The Catholic University of Korea, Seoul, Korea. parkent@dreamwiz.com
- Publication Type:Original Article
- Keywords:
TNF-a;
Otitis media with effusion;
Tumor necrosis factor;
Receptor Rats
- MeSH:
Animals;
Capillary Permeability;
Ear;
Ear, Middle;
Evans Blue;
Inflammation;
Mucous Membrane;
Otitis Media with Effusion*;
Otitis Media*;
Otitis*;
Rats;
Temporal Bone;
Tumor Necrosis Factor-alpha*;
Veins
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2000;43(9):918-924
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: lnflammatory mediators (IMs) play a major role in the production of middle ear effusion (MEE). Among the IMs detected in the MEE, tumor necrosis factor (TNF)-a seems to be important in the pathogenesis of otitis media with effusion (OME). The purposes of this study are to test the hypothesis that TNF-a in the middle ear can induce OME and that TNF-u antagonist can prevent TNF-a induced OME, and to determine the effect of TNF-c on the middle ear (ME) mucosa. MATERIALS AND METHODS: Otitis media was induced in rats by injecting TNF-a transtympanically. Other groups were treated with TNF-a after transtympanic injection of TNF-a antagonist, tumor necrosis factor soluble receptor type I (TNFsolRI), and with saline which was used as a control. Twenty-four hours after injection, ears were examined by otomicroscopy and Evans blue dye was injected into the tail vein. The temporal bones in each group were harvested and examined histopathologically and vascular permeability (VP) was measured by the Evans blue vital dye technique. RESULTS: No effusion was developed in the control group. In the TNF-a and TNF-a with TNFsolRI groups, the rate of MEE developed in the ears were 70% and 0%, respectively. A TNF-a antagonist prevented TNF-a induced OME. Histopathologic examination of middle ear revealed inflammation and mucosal thickening, an increase in the middle ear VP in the TNF-a group when compared to the other groups. CONCLUSION: This study demonstrates that TNF-a injected into the middle ear can induce OME by developing inflammation and increasing the VP of the middle ear mucosa, and that TNF-a antagonist effectively prevented TNF-a induced OME. These findings suggest that TNF-a plays an important role in the pathogenesis of OME and TNF-a antagonist may hold future therapeutic benefit in the treatment of OME.
