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嗜酸细胞凋亡在激素抵抗型哮喘中的意义 |
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ficant differences of the concentrations of both IL-5 and GM-CSF in sham cultured PBMC supernatants between SS and SR groups ［(196±68) μg/L vs. (235±98 ) μg/L IL-5 (P＞0.05), (325±110) μg/L vs. (356±131) μg/L GM-CSF (P＞0.05); SS versus SR groups, respectively］. There were statistically significant decreases in both IL-5 and GM-CSF after DXM exposure in SS group ［(196±68) μg/L vs. (147±62) μg/L IL-5 (P＜0.01); (325±110) μg/L vs.(270±97) μg/L GM-CSF (P＜0.01)］. In contrast, there were no significant differences in both IL-5 and GM-CSF after DXM exposure in SR group. Baseline rates of both EOS apoptosis and Fas antigen expression were statistically significant different between SS and SR groups ［(67±21)% vs. (33±17)% the rate of EOS apoptosis (P＜0.001); (54±23)% vs.(27±15)% the rate of Fas antigen expression (P＜0.001), SS versus SR groups, respectively］. A dramatic increase in EOS apoptosis after DXM exposure was observed in SS group ［(67±21)% vs. (89±20)% (P＜0.01), baseline vs. DXM exposure, respectively］, but there was no significant change in Fas antigen expression. There were no significant changes in both EOS apoptosis and Fas antigen expression in SR group after DXM exposure. Conclusions These data suggest that EOS compromised apoptosis might exist and could not be affected by glucocorticoid induction in SR asthma. On the other hand, Th2 cytokine over-expression could not be inhibited by glucocorticoid in SR group in vitro. 【Key words】 Asthma; Eosinophil apoptosis; Glucocorticoid resistant 依据对糖皮质激素（GC）治疗的反应性，哮喘患者可分为激素敏感型（SS）、激素依赖型（SD）与激素抵抗型（SR）。激素抵抗型患者一般病程较长，气道高反应性较严重，即使给予大剂量的糖皮质激素治疗，疗效亦不理想，临床处理较为棘手。近年来对于哮喘激素抵抗的机制进行了广泛的研究，发现此类患者T细胞及嗜酸细胞（EOS）表面GC受体的亲和力下降，单核细胞表面补体受体表达缺陷，局部存在高浓度的炎性转录因子如激活肽1（AP-1）、转录因子κB（NF-κB）等［1］。EOS作为哮喘气道炎症的主要效应细胞，其凋亡与抗凋亡机制近年倍受重视，一般认为EOS凋亡是气道炎症消退的重要途径之一，而哮喘时存在EOS凋亡不足。但EOS凋亡与激素抵抗的关系，迄今的研究甚少涉及。我们通过对一组SS和SR哮喘患者EOS凋亡现象及其调控机制的比较研究，试图了解：（1）哮喘的激素抵抗是否与EOS凋亡功能低下有关；（2）激素抵抗时促炎症细胞因子白细胞介素5（IL-5）、粒-巨噬细胞集落刺激因子（GM-CSF）的表达水平及其对EOS凋 上一页 [1] [2] [3] [4] [5] [6] 下一页
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