| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2004: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
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| Research Abstract |
In order to estimate the involvement of innate immune response in the inner ear, inflammatory cell infiltration and proinflammatory cytokine expression was investigated in the cochlea and endolymphatic sac after lipopolysaccharide (LPS), the ligand of Toll-like receptor 4, administration into peritoneal space (48 hours after injection) and middle ear (between 3 hours and 7 days after injection).
Intra-peritoneal injection of LPS induced neutrophils infiltration into perilymphatic space (p<0.01) and modiolus of the cochlea (p<0.05). Neutrophil infiltration was not observed in the control inner ear. In the endolymphatic sac, neither neutrophils nor CD68 positive cells were observed.
LPS administration into the middle ear introduced severe otitis media and the infiltrating cells expressed proinflammatory cytokines, IL1β,IL-6 and TNF-α. The LPS accessibility to the cochlea through the round window membrane is shown by previous reports. However, cochlear inflammatory cells infiltration was not evident, and proinflammatory cytokines expression was not observed neither in the cochlea nor endolymphatic sac.
Because cochlea specifically responded to intraperitoneal LPS administration, the innate immune system could work in cochlea. But less cochlear response to LPS comparing to the middle ear might related with the sensitivity to LPS in the inner ear. Innate immune system might not play major role in the inner ear.
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