MECHANISMS OF STRESS-INDUCED MODULATION OF VIRAL PATHOGENESIS AND IMMUNITY
MECHANISMS OF STRESS-INDUCED MODULATION OF VIRAL PATHOGENESIS AND IMMUNITY
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DOI：
10.1016/0165-5728(93)90187-4
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发表时间：
1993-11-01
影响因子：
3.3
通讯作者：
SHERIDAN, JF
中科院分区：
文献类型：
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作者：
DOBBS, CM;VASQUEZ, M;SHERIDAN, JF
用单纯疱疹病毒（HSV）感染的小鼠模型研究了儿茶酚胺和皮质酮在束缚应激诱导的病毒免疫抑制中的作用。用糖皮质激素受体拮抗剂RU 486治疗C57 BL/6小鼠，逆转了应激诱导的细胞结构减少对局部HSV感染的反应。用纳多洛尔（一种外周作用的β-肾上腺素能拮抗剂）和RU 486治疗小鼠完全逆转了束缚应激诱导的HSV特异性CTL激活抑制。这些发现表明，皮质酮和儿茶酚胺介导的机制是有效的应激诱导的抗病毒细胞免疫抑制。
A murine model of herpes simplex virus (HSV) infection was used to examine the roles of catecholamines and corticosterone in the restraint stress-induced suppression of viral immunity. Treatment of C57BL/6 mice with RU486, a glucocorticoid receptor antagonist, reversed the stress-induced diminution of cellularity in response to local HSV infection. Treatment of mice with both nadolol, a peripherally acting beta-adrenergic antagonist, and RU486 completely reversed the restraint stress-induced suppression of HSV-specific CTL activation. These findings demonstrate that both corticosterone and catecholamine-mediated mechanisms are operative in the stress-induced suppression of anti-viral cellular immunity.