地塞米松抑制IL-5诱导的嗜酸粒细胞的存活

Dexamethasone Inhibits IL 5 Induced Eosinophil Survival

目的通过地塞米松对白介素－５（ＩＬ－５）诱导的ＥＯＳ存活的影响，探讨地塞米松治疗哮喘的作用机制。方法将外周血的ＥＯＳ加入ＩＬ－５和不同浓度的ＤＥＸ共同培养，以观察ＤＥＸ对ＩＬ－５诱导的ＥＯＳ存活的作用。结果大于５ｐｇ／ｍｌ水平的ＩＬ－５明显提高ＥＯＳ的存活，且有剂量依赖性；Ｄｅｘ以剂量依赖的方式抑制ＥＯＳ的存活，从５０ｎｍｏｌ／Ｌ开始，１０００ｎｍｏｌ／Ｌ的Ｄｅｘ抑制达到最强；而当ＩＬ－５浓度为１００ｐｇ／ｍｌ或更高时，其诱导的ＥＯＳ存活不能被任何浓度的ＤＥＸ所抑制。Ｄｅｘ对ＥＯＳ存活的作用有时间依赖性，其抑制作用在高浓度的ＩＬ－５存在条件下可延迟或消失。结论Ｄｅｘ对疾病的治疗可能存在着抵抗。

Objective To assess the effect of dexamethasone (Dex) on interleukine 5 induced survival of eosinophils (EOS) in vitro. Methods EOS were purified from guinea pigs by Percoll density gradient and incubated for 4 days in the presence of IL 5 with or without Dex. Cell viabilities were determined by staining cells with fluorescein diacetate and propidium iodide. Results In the absence of Dex, IL 5 enhanced EOS survival was inhibited in a dosedependent manner.Inhibition was time dependent and required at least 2 days exposure of EOS to Dex. When EOS were incubated with varying concentrations of IL 5 and 1 000 nmol/l Dex, survival inhibition was reduced at higher concentration of IL 5, and completely abolished by IL 5 1 000 pg/ml. Conclusions Dex acts directly on mature EOS to decrease their viabilities, implying the Dex may be important in the treatment of allergic and other inflammatory eosinophilic disorders.