Department of Nursing, Chang Gung Institute of Technology, 261 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan, Taiwan, 333, Republic of China.
J Clin Immunol. 2011 Aug;31(4):656-65. doi: 10.1007/s10875-011-9529-3. Epub 2011 Jun 4.
In this study, we evaluated the anti-inflammatory response and the mechanism by which dehydroepiandrosterone modulates immunity in ovalbumin-sensitized asthmatic mice. Female BALB/c mice were sensitized and challenged with ovalbumin and then treated with oral administration of dehydroepiandrosterone on days 21 to 27. The results showed dehydroepiandrosterone could suppress airway hyperresponsiveness and decrease eosinophil infiltration of the lungs in ovalbumin-sensitized mice. Moreover, dehydroepiandrosterone inhibited chemokines, including CCL11/eotaxin-1 and CCL24/eotaxin-2, and Th2-associated cytokine levels in bronchoalveolar lavage fluid. After the inflammatory human bronchial epithelial cell line BEAS-2B was treated with dehydroepiandrosterone, levels of proinflammatory cytokines and chemokines were inhibited, including IL-6, IL-8, CCL11, and CCL24. We suggested that dehydroepiandrosterone inhibited inflammation in bronchial epithelial cells as indicated by the suppression of Th2-associated cytokines and chemokines. Dehydroepiandrosterone also suppressed eosinophil migration and infiltration into the lung to improve the symptoms of asthma in ovalbumin-sensitized mice.
在这项研究中，我们评估了脱氢表雄酮（DHEA）调节卵清蛋白致敏哮喘小鼠免疫的抗炎反应及其机制。雌性 BALB/c 小鼠经卵清蛋白致敏和激发后，在第 21 至 27 天给予 DHEA 口服治疗。结果表明，DHEA 可抑制气道高反应性并减少卵清蛋白致敏小鼠肺部嗜酸性粒细胞浸润。此外，DHEA 抑制趋化因子，包括 CCL11/eotaxin-1 和 CCL24/eotaxin-2，以及支气管肺泡灌洗液中 Th2 相关细胞因子水平。在炎性人支气管上皮细胞系 BEAS-2B 用 DHEA 处理后，促炎细胞因子和趋化因子的水平被抑制，包括 IL-6、IL-8、CCL11 和 CCL24。我们认为 DHEA 通过抑制 Th2 相关细胞因子和趋化因子抑制了支气管上皮细胞的炎症。DHEA 还抑制嗜酸性粒细胞向肺部的迁移和浸润，从而改善卵清蛋白致敏小鼠的哮喘症状。
