STRESS-INDUCED FEVER--ROLE OF CYTOKINES AND HORMONES

压力引起的发烧——细胞因子和激素的作用

• 批准号: 2415963
• 负责人: MATTHEW J KLUGER
• 金额: $ 9.15万
• 依托单位: LOVELACE RESPIRATORY RESEARCH INSTITUTE
• 依托单位国家: 美国
• 财政年份: 1991
• 资助国家: 美国
• 起止时间: 1991-08-01 至 1997-09-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2415963
• 关键词: behavioral /social science research tag; beta adrenergic agent; cytokine; glucocorticoids; interleukin 6; laboratory rat; psychological stressor; psychoneuroimmunology; psychopharmacology

DESCRIPTION (Adapted from applicant's abstract): Exposure to psychosocial stress produces rises in body temperature of as much as 2oC in rats. The applicant has generated data that support the hypothesis that stress "hyperthermia" is actually a fever (i.e. an elevation in thermoregulatory set point), caused by endogenous pyrogens and prostanoids. Cytokines are released during stress-induced fevers and the applicant has found that exposing a rat to a novel environment results in an increase in concentrations of IL-6, a mediator of inflammation and immunity. Pretreatment with antiserum to TNF-alpha results in an increase of stress fevers. Evidence is also presented that adrenalectomized rats develop larger stress-induced fevers and increased plasma concentrations of IL-6 which is reversed when replacement corticosterone is given. Infusion of RU38486 into the anterior hypothalamus suggests that glucocorticoid negative feedback on stress induced fever and IL-6 rises occur at the level of the central nervous system. Furthermore, injection of beta-adrenoceptor blockers into the CNS attenuates both stress-induced fevers and the rise of IL-6 cytokines. The aims of this study are to: 1) determine the role and site of action of beta-adrenoceptors in modulating stress-induced rises in body temperature and circulating cytokines; and 2) determine the role and site of action of circulating glucocorticoids in modulating stress-induced rises in body temperature and circulating cytokines.

描述（改编自申请人摘要）：暴露于社会心理 压力会使老鼠的体温上升2摄氏度。 的 申请人已经生成了支持以下假设的数据： “体温过高”实际上是发烧（即体温调节的升高）。 设定点），由内源性热原和前列腺素类引起。 细胞因子是 在压力引起的发烧期间释放，并且申请人已经发现， 将大鼠暴露于新环境会导致 IL-6是炎症和免疫的介质。 用TNF-α抗血清预处理导致应激增加 发烧 也有证据表明，肾上腺切除大鼠发展 更大的应激诱导发热和IL-6的血浆浓度增加 当给予皮质酮替代品时，这种情况会逆转。 输注 RU 38486进入下丘脑前部表明糖皮质激素阴性 对应激诱导的发热和IL-6升高的反馈发生在 中枢神经系统 此外，注射β-肾上腺素受体 阻滞剂进入中枢神经系统减弱应激诱导的发热和 IL-6细胞因子。 本研究的目的是：1）确定角色， β-肾上腺素受体在调节应激诱导的 体温和循环细胞因子;和2）确定作用， 循环糖皮质激素在调节应激诱导的 体温和循环细胞因子升高。