Department of Microbiology and Immunology, Graduate Institute of Biomedical Science, Chang Gung University, 259 Wen-Hwa 1st Road, Kwei-Shan, Tao-Yuan 333, Taiwan, ROC.
J Dermatol Sci. 2013 Nov;72(2):149-57. doi: 10.1016/j.jdermsci.2013.06.015. Epub 2013 Jul 9.
Th2 cells are overexpressed in the skin and serum of atopic dermatitis (AD) patients. Previously, we found that dehydroepiandrosterone (DHEA) decreased eosinophil infiltration in asthmatic mice through the suppression of Th2-associated cytokines. Therefore, we hypothesized that DHEA might improve the symptoms of AD syndrome.
In this study, we evaluated the symptom improvement and anti-inflammatory response that result from the modulation of immunity by DHEA modulated in AD-like mice.
Female BALB/c mice were sensitized and challenged with 1-chloro-2,4-dinitrobenzene. On days 14-29 after sensitization, mice were treated with cutaneous (skin smear) or oral administration of DHEA. In addition, human keratinocyte (HaCat) cells were used to evaluate the effect of DHEA on the in vitro production of proinflammatory cytokines and chemokines.
Both cutaneous and oral DHEA were able to decrease ear swelling and skin inflammation in AD-like mice. DHEA also attenuated eosinophil and mast cell infiltration into ear and skin tissue. Additionally, Th2-associated cytokines were inhibited in splenocyte culture, and suppressed the levels of IgE and interleukin 4 in serum. Oral and cutaneous administration of DHEA reduced the inflammatory response, as evidenced by AD-like skin lesions, in a similar manner. DHEA significantly reduced inflammatory cytokines and chemokines through the nuclear factor-κB and mitogen-activated protein kinases pathways in tumor necrosis factor-α activated HaCat cells.
DHEA ameliorates AD-like mouse skin inflammation and reduces eosinophil and mast cell infiltration by reducing the production of Th2-associated cytokines and chemokines.
特应性皮炎（AD）患者的皮肤和血清中 Th2 细胞过度表达。此前，我们发现脱氢表雄酮（DHEA）通过抑制 Th2 相关细胞因子减少哮喘小鼠中的嗜酸性粒细胞浸润。因此，我们假设 DHEA 可能改善 AD 综合征的症状。
在这项研究中，我们评估了 DHEA 通过调节 AD 样小鼠的免疫来改善症状和抗炎反应。
雌性 BALB/c 小鼠用 1-氯-2,4-二硝基苯致敏和攻击。致敏后第 14-29 天，用皮肤（皮肤涂片）或口服 DHEA 治疗小鼠。此外，还使用人角质形成细胞（HaCat）细胞评估 DHEA 对体外产生促炎细胞因子和趋化因子的影响。
皮肤和口服 DHEA 均可减轻 AD 样小鼠的耳部肿胀和皮肤炎症。DHEA 还减弱了嗜酸性粒细胞和肥大细胞向耳部和皮肤组织的浸润。此外，在脾细胞培养中抑制 Th2 相关细胞因子，并降低血清中 IgE 和白细胞介素 4 的水平。口服和皮肤给予 DHEA 以相似的方式减轻 AD 样皮肤病变，表明减轻了炎症反应。DHEA 通过肿瘤坏死因子-α激活的 HaCat 细胞中的核因子-κB 和丝裂原激活的蛋白激酶途径显著减少炎症细胞因子和趋化因子。
DHEA 通过减少 Th2 相关细胞因子和趋化因子的产生，改善 AD 样小鼠皮肤炎症并减少嗜酸性粒细胞和肥大细胞浸润。
