| Research Abstract |
In the present study, the role of eosinophil infiltration on the expansion of intractable allergic diseases were studied, using allergic rhinitis models and rat peritoneal mast cells. When the sensitized mast cells were stimulated with antigen, the increase of expression of MIP-1 α, IL-6 and MCP-1 mRNA were observed, time-dependently. The expression of MIP- 1 α and IL-6 mRNA was declined by catalase. Hydrogen peroxide also stimulated the expression of MIP-1 α and IL-6 mRNA in mast cells. When histamine was dropped on the nasal mucosa of guinea pigs, the maximal increase of eosinophil infiltration was observed at 24 h after. The tine-course of infiltration was similar to that of infiltration after antigen challenge. The increase of eosinophil infiltration was prevented by the pretreatment with ebastine, a histamine H1 antagonist. These findings suggested that histamine, a chemical mediator of an early phase, may contribute to the eosinophil infiltration. Next, the rats, passively sensit
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ized with anti-ovalbumin serum which was prepared in BN rats were used. 6 hrs after the sensitization, antigen was inhalated for 2 min. The nasal mucosa was removed at 1 hr, 3 hrs, 6 hrs and 12 hrs after the inhalation, and mRNA was prepared. The expression of several cytokines mRNA was analysed with RT-PCR amplification, using the primer of MIP- 1α, eotaxin, RANTES and MCP-1. MIP-1 α mRNA was not expressed in the non-sensitized and the sensitized rats, but eotaxin mRNA was already expressed in the non-sensitized rats and the expression was enhanced by the sensitization. The expression of RANTES and MCP-1 mRNA was observed, constantly. The application of antigen to the sensitized rats remarkablely elicited the expression of MIP-1 α mRNA 1 hr after, and the expression declined time-dependently. However, the increase of expression was observed at 12 hrs after again. The time-dependent change of eotaxin mRNA was not observed after antigen challenge. Lymphocytes, collected in the effluent of nasal cavity, changed to CD3 possitive cells, T lymphocytes, after antigen challenge. And the T lymphocytes were CD4 negative and γ δ TCR negative. Less
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