Nair M P, Saravolatz L D, Schwartz S A
Department of Medicine and Microbiology, State University of New York at Buffalo, Buffalo General Hospital 14203, USA.
Immunol Invest. 1995 Aug;24(5):689-99. doi: 10.3109/08820139509060698.
To examine the potential role of stress hormones in the progression of HIV infections, we developed an in vitro model system that investigates the effects of cortisol, adrenocorticotropin-releasing hormone (ACTH) and beta-endorphin on the natural killer cell activity of lymphocytes from normal subjects and AIDS patients. The system employs a 4 hr 51Cr release assay and K562 target cells. Direct addition of cortisol (0.05, 0.1, and 0.2 microgram/ml) or ACTH (10(-6) to 10(-8) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of normal lymphocytes. Direct addition of beta-endorphin (10(-13) to 10(-17) M) to the mixture of effector and prelabeled target cells did not produce any significant immunoregulatory effects on the NK cell activity of lymphocytes from normal or AIDS subjects. However, cortisol and ACTH significantly inhibited the NK activity of lymphocytes from AIDS patients. The selective inhibitory effects of cortisol and ACTH in patients with HIV infections are consistent with a model which proposes that stress related neurohormones and/or neuropeptides may be involved in the progression of HIV infections.
为了研究应激激素在HIV感染进展中的潜在作用，我们开发了一种体外模型系统，该系统可研究皮质醇、促肾上腺皮质激素释放激素（ACTH）和β-内啡肽对正常受试者和艾滋病患者淋巴细胞自然杀伤细胞活性的影响。该系统采用4小时51Cr释放试验和K562靶细胞。将皮质醇（0.05、0.1和0.2微克/毫升）或促肾上腺皮质激素（10^(-6)至10^(-8)M）直接添加到效应细胞和预先标记的靶细胞混合物中，对正常淋巴细胞的NK细胞活性未产生任何显著的免疫调节作用。将β-内啡肽（10^(-13)至10^(-17)M）直接添加到效应细胞和预先标记的靶细胞混合物中，对正常或艾滋病受试者淋巴细胞的NK细胞活性未产生任何显著的免疫调节作用。然而，皮质醇和促肾上腺皮质激素显著抑制了艾滋病患者淋巴细胞的NK活性。皮质醇和促肾上腺皮质激素对HIV感染患者的选择性抑制作用与一种模型一致，该模型提出与应激相关的神经激素和/或神经肽可能参与了HIV感染的进展。
