Role of Interleukin-10 on Mouse Otitis Media Model Using Lipopolysaccharide / 대한이비인후과학회지
Korean Journal of Otolaryngology - Head and Neck Surgery
;
: 43-47, 2011.
Artículo
en Coreano
| WPRIM
| ID: wpr-652110
ABSTRACT
BACKGROUND AND OBJECTIVES:
Interleukin (IL)-10 is a major regulator of innate immunity. It interferes with the production of inflammatory mediators by reacting with polymorphonuclear neutrophils, monocytes and macrophages. In addition, it also up-regulates the ex-pression of molecules that amplify the anti-inflammatory effect of IL-10. This study tested the hypothesis that injection of various concentrations of exogenous IL-10 in the middle ear cleft can inhibit the acute stage of otitis media induced by lipopolysaccharide (LPS). And if so, the level of concentration for inhibition can be determined. MATERIALS ANDMETHOD:
IL-10 and/or LPS were injected transtympanically into the middle ear cavity of normal mice. Histopathological measurement of submucosal thickness and num-ber of inflammatory cell infiltration was performed at 24 hours after inoculation of IL-10 and/or LPS.RESULTS:
At 24 hours after inoculation, every group of IL-10 inoculation reduced both thickening of the mucous and submucosal infiltration of inflammatory cells in a dose-dependent manner. As the concentrations of IL-10 inoculated increased, mucosal thickness and submucosal infiltration of inflammatory cells were more reduced.CONCLUSION:
This study demonstrated that exogenous IL-10 injection into the middle ear can directly reduce LPS-induced otitis media in acute stage in a dose-dependent manner. These findings also indicate that IL-10 may be a candidate for local modulator of acute otitis media.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Otitis
/
Otitis Media
/
Monocitos
/
Interleucinas
/
Interleucina-10
/
Oído Medio
/
Inmunidad Innata
/
Macrófagos
/
Neutrófilos
Tipo de estudio:
Estudio pronóstico
Límite:
Animales
Idioma:
Coreano
Revista:
Korean Journal of Otolaryngology - Head and Neck Surgery
Año:
2011
Tipo del documento:
Artículo
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