A warmer ambient temperature increases the passage of interleukin-1β into the brains of old rats
A warmer ambient temperature increases the passage of interleukin-1β into the brains of old rats
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DOI：
10.1152/ajpregu.00104.2007
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发表时间：
2008-07-01
影响因子：
2.8
通讯作者：
Satinoff, Evelyn
中科院分区：
文献类型：
--
作者：
Buchanan, Jessica B.;Peloso, Elizabeth;Satinoff, Evelyn
我们已经证明，腹腔内注射脂多糖（LPS）后，老年大鼠在31℃的环境温度（Ta）下会出现与年轻大鼠相似的发烧，但在21℃时则不会。腹腔内或静脉注射IL-1β也是如此。老年大鼠发热迟缓的根本机制可能是外周和大脑之间的沟通缺陷。老年大鼠的外周细胞因子作用可能发生改变，从而导致到达大脑的信号减弱。在这里，我们假设在标准实验室温度下，没有足够的 IL-1 β 到达大脑而导致发烧，而温度升高会增加 IL-1 β 流入大脑的数量，从而使老年大鼠发烧。将年轻（3-5 个月）和老年（23-29 个月）Long-Evans 大鼠在 Ta 21 摄氏度或 31 摄氏度下维持 3 天，然后静脉注射放射性标记的 IL-1 β 以测量穿过血脑屏障的情况。年轻大鼠在两个 Tas 时表现出类似的 IL-1 β 流入大脑，但老年大鼠仅在较温暖的 Ta 时表现出显着的流入。这些数据表明，凉爽时不发烧可能是由于流入大脑的 IL-1 β 减少所致。
We have demonstrated that after intraperitoneal lipopolysaccharide ( LPS) injection, old rats mount fevers similar to those of young rats at an ambient temperature ( Ta) of 31 degrees C, but not at 21 degrees C. The same is true for intraperitoneal or intravenous IL-1 beta administration. The underlying mechanism responsible for blunted fever in old rats may be a deficiency in communication between the periphery and the brain. Possibly, peripheral cytokine actions are altered in old rats, such that the signal that reaches the brain is diminished. Here, we hypothesized that at standard laboratory temperatures, not enough IL-1 beta is reaching the brain for fever to occur and that a warmer Ta would increase the influx of IL-1 beta into the brain, enabling old rats to generate fever. Young (3-5 mo) and old ( 23-29 mo) Long-Evans rats were maintained for 3 days at either Ta 21 degrees or 31 degrees C prior to intravenous injection with radiolabeled IL-1 beta to measure passage across the blood-brain barrier. Young rats showed similar influx of IL-1 beta into the brain at the two Tas, but old rats showed significant influx only at the warmer Ta. These data suggest that the lack of fever at a cool Ta may be due to a reduced influx of IL-1 beta into the brain.