| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
Eosinophils (Eos) play an important role in the pathogenesis of bronchial asthma. However, it is unclear by what or how eosinophil degranulation is induced in vivo.
In 1998, we performed the basic examination on human eosinophil degranulation in the presence of bronchial epithelial cells (Ep). The results were as follows. In coculture of Eos and Ep without stimulus, 298±34ng/10^6Eos(n=5) were released spontaneously. When we examined the adhesion of Eos to Ep, eosinophil adhesion was 9.0±0.9% in coculture without stimulus. When Eos alone were activated or whet Ep alone were activated, no significant enhancement of eosinophil adhesion was observed.
In 1999, we examined the stimulus effects of cytokines and immunoglobulins on ECP release and eosinophil adhesion. The results were as follows. Coculture of Eos and Ep with IL-5 treatment and TNF treatment, respectively, resulted in the enhancement of ECP release and eosinophil adhesion. The enhancement of ECP release was partially inhibited by anti-CD 18 mAb, which caused comparable inhibition on the potentiation of eosinophil adhesion. In the presence of Ep coated by IgG1, ECP release was significantly enhanced in comparison with non-coated Ep. In the presence of Ep coated by IgG2, IgG3, IgG4, sIgA, IgE or IgM, no significant enhancement of ECP release was observed. Therefore, it is suggested that epithelial cell activation and IgG1 influence eosinophil degranulation in the presence of Ep and that adhesion molecules may be involved in the mechanism.
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