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Interleukin-1beta-induced fever in young and old Long-Evans rats.

机译:白细胞介素-1β诱导的老年和老年Long-Evans大鼠发烧。

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摘要

Aging is associated with a blunted or absent fever response to naturally occurring infections or to the peripheral administration of bacterial products and proinflammatory cytokines, including interleukin-1beta (IL-1beta). Whether old rats also exhibit an attenuated fever response when challenged with direct brain administration of IL-1beta is unknown. Here we investigated the fever response of young (3-5 mo) and old (24-26 mo) Long-Evans rats to the intracerebroventricular microinfusion of IL-1beta. Core body temperature was monitored by telemetry in freely moving rats. Intracerebroventricularly administered IL-1beta induced comparable increases in body temperature in young and old Long-Evans rats. In the two groups, IL-1beta-induced fever was similar both in latency to peak fever and maximal fever response, whether the cytokine was administered 2 h after lights on or just before lights off. These data show that old Long-Evans rats are not defective in their capacity to develop a fever in response to brain administration of IL-1beta.
机译:衰老与对自然感染或对细菌产物和促炎性细胞因子(包括白介素-1β(IL-1beta))的外周给药产生的发烧反应迟钝或不相关。尚不知道当直接向大脑注射IL-1β攻击时,老年大鼠是否也表现出减弱的发烧反应。在这里,我们调查了年轻(3-5个月)和老龄(24-26个月)Long-Evans大鼠对脑室内微输注IL-1beta的发烧反应。通过遥测在自由移动的大鼠中监测核心体温。脑室内给予的IL-1β可以诱导年老的Long-Evans大鼠的体温升高。在两组中,无论是在开灯后2小时还是在开灯前施用细胞因子,IL-1β诱导的发烧在潜伏期都与峰值发烧和最大发烧反应相似。这些数据表明,长的Long-Evans大鼠在响应于IL-1β的脑部给药后发烧的能力没有缺陷。

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