Racial differences in T-lymphocyte response to glucocorticoids
Racial differences in T-lymphocyte response to glucocorticoids
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DOI：
10.1378/chest.127.2.571
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发表时间：
2005-02-01
期刊：
影响因子：
9.6
通讯作者：
Spahn, JD
中科院分区：
文献类型：
--
作者：
Federico, MJ;Covar, RA;Spahn, JD
背景：黑人哮喘的发病率和死亡率较高。
目的：这项横断面研究的主要目的是确定黑人（无论是否患有哮喘）在体外对糖皮质激素的T淋巴细胞反应是否比白人减弱。如果发现差异，这将表明黑人存在糖皮质激素反应性降低的种族倾向。
方法：从美国国立犹太医学研究中心及周边社区招募的哮喘患者（n = 395，其中27%为黑人）和对照组（n = 202，其中52%为黑人）参与了研究。通过评估抑制植物血凝素诱导的T淋巴细胞增殖50%所需的地塞米松浓度的对数转换值（log(10) IC50）来确定体外糖皮质激素反应性。收集了哮喘用药史、特应性状态以及针对种族校正的肺功能肺活量测定指标。
结果：黑人和白人哮喘患者的第一秒用力呼气容积（FEV1）、预测值百分比以及吸入和口服糖皮质激素的需求量相似。与白人哮喘患者相比，黑人哮喘患者的糖皮质激素反应性显著降低，具体如下：log(10) IC50值的中位数（第一四分位数，第三四分位数）为1.00纳摩尔（0.48，1.83）对比0.78纳摩尔（0.29，1.45）[p = 0.028]。在黑人和白人对照组之间也发现了类似结果，如下：中位数为1.26纳摩尔（0.70，2.14）对比0.95纳摩尔（0.55，1.48）[p = 0.01]。年龄、种族和基础T淋巴细胞活性与log(10) IC50值呈显著正相关。
结论：我们观察到黑人哮喘患者和非哮喘对照组在体外抑制T淋巴细胞活化需要更高浓度的糖皮质激素，这表明黑人存在糖皮质激素反应性降低的种族倾向，这可能导致他们哮喘发病率升高。
Background: Asthma morbidity and mortality is increased in blacks.Objective: The primary objective of this cross-sectional study was to determine if blacks, asthmatic or nonasthmatic, displayed diminished T-lymphocyte response to glucocorticoids in vitro compared to their white counterparts. If differences were noted, this would suggest a racial predisposition to decreased glucocorticoid responsiveness among blacks.Methods: Asthmatic (n = 395, 27% blacks) and control (n = 202, 52% blacks) subjects recruited from National Jewish Medical and Research Center and from the surrounding community participated in the study. In vitro glucocorticoid responsiveness was determined by assessing the log-transformed concentration of dexamethasone required to suppress phytohemagglutinin-induced T-lymphocyte proliferation by 50% (log(10) IC50). Asthma medication history, atopic status, and spirometric lung function measures corrected for race were collected.Results: Black and white asthmatic subjects had similar FEV1, percentage of predicted values and inhaled and oral glucocorticoid requirements. Black asthmatic subjects displayed significantly diminished glucocorticoid responsiveness compared to white asthmatic subjects, as follows: median (first, third quartile) log(10) IC50 values of 1.00 nmol (0.48, 1.83) vs 0.78 nmol (0.29, 1.45) [p = 0.028]. Similar results were found between black and white control subjects, as follows: median, 1.26 nmol (0.70, 2.14) vs 0.95 - nmol (0.55, 1.48) [p = 0.01]. Age, race, and basal T-lymphocyte activity were significantly positively correlated to the log(10) IC50 values.Conclusion: Our observation that black asthmatic subjects and non-asthmatic control subjects require greater concentrations of glucocorticoid in vitro to suppress T-lymphocyte activation suggests that blacks have a racial predisposition to diminished glucocorticoid responsiveness, which may contribute to their heightened asthma morbidity.