| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Research Abstract |
We examined the role of tumor necrosis factor alpha (TNFalpha), interleukin-1 (IL-1), interleukin-8 (IL-8) in the mediation of increased vascular permeability in rabbits with LPS-induced pleurisy. The increased vascular permeabitlity was composed of two phases : immediate (15 min) and delayd (2 hr). The immediate permeability was inhibited by H1-antihistamine but was not affected by anti-TNFalpha, by interleukin-1 receptor antagonist (IL-1ra), by anti-IL-8, or by depletion of neutrophils. The delayd permeability was inhibited by anti-TNFalpha, by anti-IL-8, or by depletion of neutrophils, and was not affected by IL-1ra or antihistamine. Maximal levels of TNFalpha and IL-8 were detected in pleural fluid at 2 h after LPS-injection. Production of IL-8 in LPS-pleurisy was inhibited with anti-TNFalpha, whereas the production of TNFalpha was not affected with anti-IL-8. Injection of homologous IL-8 induced VP of which time-course preceded that of LPS-induced delayd VP.Injection of IL-8 did not induce TNFalpha production and anti-TNFalpha had no effect on IL-8-induced VP.Injection of homologous TNFalpha induced IL-8 production and VP,and TNFalpha-induced delayd VP was blocked with anti-IL-8. These results indicate important roles of IL-8 in LPS-induced delayd VP and plasma leakage induced by TNFalpha appears to be dependent on secondary production of IL-8.
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