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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

基本信息

批准号：
2829198
负责人：
MATTHEW J KLUGER
金额：
$ 21.81万
依托单位：
LOVELACE BIOMEDICAL & ENVIRONMENTAL RESEARCH INSTITUTE
依托单位国家：
美国
项目类别：
财政年份：
1991
资助国家：
美国
起止时间：
1991-08-01 至 2000-04-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/2829198
关键词：
behavioral /social science research tag beta adrenergic agent cytokine glucocorticoids interleukin 6 laboratory rat psychological stressor psychoneuroimmunology psychopharmacology

项目摘要

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应激诱导的发烧加剧和血浆IL-6浓度升高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。