RT期刊文章SR电子T1糖皮质激素对释放的影响的咆哮和sICAM-1培养人类支气管上皮细胞,引起tnf摩根富林明欧洲呼吸杂志乔和J FD欧洲呼吸学会SP 834欧元OP 840签证官是4 A1王,JH A1 Devalia, JL A1 Sapsford, RJ A1戴维斯,188bet官网地址我们最近证实了人支气管上皮细胞可以合成和释放多种炎症介质，包括调节活化的因子，正常t细胞表达和分泌(RANTES)和可溶性细胞间黏附分子-1 (sICAM-1)，它们影响嗜酸性粒细胞的活性，因此可能在哮喘的病因学中发挥作用。在这项研究中，我们研究了糖皮质激素是否能够影响这些促炎介质从人支气管上皮细胞的释放。人支气管上皮细胞培养融合为外植体培养，并在50ng x mL(-1)肿瘤坏死因子- α (tnf - α) +/- 0-10(-4) M丙酸氟替卡松(FP)、二丙酸倍氯米松(BDP)、或氢化可的松(HC)培养24 h。收集培养液，通过酶联免疫吸附试验(ELISA)分析RANTES和sICAM-1，并分析细胞的总蛋白。tnf - α显著增加RANTES和sICAM-1的释放(63.0 fg RANTES x microg(-1)蛋白;p < 0.05;8.8 pg sICAM-1 x microg(-1)蛋白;p<0.02)，与未处理细胞相比(10.3 fg RANTES x microg(-1)蛋白; 2.6 pg sICAM-1 x microg(-1) cellular protein). The TNF-alpha-induced release both of RANTES and sICAM-1 occurred in a time-dependent manner, and was maximal by 24 h incubation. FP 10(-6)-10(-4) M significantly attenuated the TNF-alpha-induced release both of RANTES and sICAM-1. In contrast, 10(-4) M BDP or HC significantly attenuated the release of only sICAM-1. These results suggest that corticosteroids may prevent airway inflammation by downregulating the synthesis and/or release of proinflammatory mediators from bronchial epithelial cells. Furthermore, fluticasone propionate may be more efficacious than beclomethasone dipropionate or hydrocortisone in this respect.