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Proinflammatory cytokines expression in noise-induced damaged cochlea

Masato Fujioka, Sho Kanzaki, Hirotaka James Okano +5 more2006Journal of Neuroscience ResearchJournal Article
10.1002/jnr.20764PubMed
Immune/InnateNeurological

Abstract

Recent studies have showed that inflammatory responses occur in inner ear under various damaging conditions including noise-overstimulation. We evaluated the time-dependent expression of proinflammatory cytokines in noise-exposed rat cochlea. Among several detected cytokines, real-time RT-PCR showed that interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) were significantly induced 3 hr after noise exposure, and quickly downregulated to the basal level. Tumor necrosis factor-alpha (TNF-alpha) was also slightly upregulated immediately after noise exposure. Immunohistochemical analysis showed that IL-6 expression was distinctively induced within the lateral side of the spiral ligament. Sequential expression analysis showed that IL-6 immunoreactivity was initially found in the cytoplasm of lateral wall cells, including Type IV and III fibrocytes, and expanded broader throughout the lateral wall, finally to the stria vascularis. Because of the negative Iba-1 staining, IL-6 expression in the early-phase was not due to macrophage or microglia activation. IL-6 was also detected in spiral ganglion neurons at 12 and 24 hr after noise exposure. Our data demonstrates the production of proinflammatory cytokines, including TNF-alpha, IL-1beta, and IL-6, in early phase of noise overstimulated cochlea. IL-6 expression was observed in the spiral ligament, stria vascularis, and spiral ganglion neurons. These cytokines, produced by the cochlear structure itself in response to noise exposure, may initiate an inflammatory response and have some role in the mechanism of noise-induced cochlear damage.

Key Biomarkers

Interleukin-1β (IL-1β)Interleukin-6 (IL-6)Tumor necrosis factor-alpha (TNF-α)

Symptom Clusters

Inner ear inflammationNoise-induced cochlear damage

Cited By (6)

  • Oxidative stress, inflammation, and autophagic stress as the key mechanisms of premature age-related hearing loss in SAMP8 mouse cochleaAntioxidants and Redox Signaling · 2012
  • Dexamethasone protects organ of corti explants against tumor necrosis factor-alpha–induced loss of auditory hair cells and alters the expression levels of apoptosis-related genesNeuroscience · 2008
  • Blocking pro-cell-death signal pathways to conserve hearingAudiology and Neurotology · 2009
  • Expression of the proinflammatory cytokines in cochlear explant cultures: influence of normoxia and hypoxiaNeuroscience Letters · 2010
  • The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotective strategiesRecent Patents on CNS Drug Discovery · 2010
  • Okano H. blockade of interleukin-6 signaling suppressed cochlear inflammatory response and improved hearing impairment in noise-damaged mice cochleaNeurosci Res · 2010

References (1)

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