Expression and Distribution of Tumor Necrosis Factor-Alpha in Mice Cochlea Exposed to Noise.
10.3342/kjorl-hns.2010.53.9.527
- Author:
Min Ho JO
1
;
Chang Ju KIM
;
Seung Hyun KOH
;
Gi Sung NAM
;
Ha Min JEONG
;
Jae Hoon LEE
;
Sang Heon LEE
Author Information
1. Department of Otolaryngology-Head and Neck Surgery, Wonkwang University College of Medicine, Iksan, Korea. pericomo@wku.ac.kr
- Publication Type:Original Article
- Keywords:
Noise-induced hearing loss;
Cytokines;
Tumor necrosis factor-alpha
- MeSH:
Animals;
Cochlea;
Cytokines;
Ear, Inner;
Hearing Loss, Noise-Induced;
Immunohistochemistry;
Inflammation;
Mice;
Noise;
Spiral Ganglion;
Stria Vascularis;
Tumor Necrosis Factor-alpha
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2010;53(9):527-533
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND OBJECTIVES: Recent studies have shown that inflammatory responses occur in the inner ear under various damaging conditions including noise-overstimulation.Identification of time-dependent expression patterns of pro-inflammatory cytokines during the response initiation should lead to rational therapeutic strategies that block the response and reduce the damaging sequelae. MATERIALS AND METHOD: We evaluated the time-dependent expression pattern of pro-inflammatory cytokines in noise-exposed mouse cochlea (white noise, 120 dB SPL, 3 hours) using immunohistochemistry and reverse transcriptase-polymerase chain reaction(RT-PCR). RESULTS: The most potent pro-inflammatory cytokine, the tumor necrosis factor-alpha (TNF-alpha), was up-regulated after noise exposure. Immunohistochemical analyses showed that the TNF-alpha expression was distinctively induced within the spiral ganglion and stria vascularis. RT-PCR showed that TNF-alpha was induced shortly after noise exposure and persisted upto seven days following noise exposure. CONCLUSION: Taken together, acoustic trauma induces cochlear inflammation and the data suggest that TNF-alpha may have some role in cochlea damage that occur following noise exposure.