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A warmer ambient temperature increases the passage of interleukin-1β into the brains of old rats

机译:环境温度升高会增加白细胞介素-1β进入老年大鼠大脑的通道

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摘要

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°C, but not at 21°C. The same is true for intraperitoneal or intravenous IL-1β 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-1β is reaching the brain for fever to occur and that a warmer Ta would increase the influx of IL-1β 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 or 31°C prior to intravenous injection with radiolabeled IL-1β to measure passage across the blood-brain barrier. Young rats showed similar influx of IL-1β 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-1β into the brain.
机译:我们已经证明,腹膜内注射脂多糖(LPS)后,老年大鼠在31°C的环境温度(Ta)而非21°C会发烧,类似于年轻大鼠的发烧。对于腹膜内或静脉内IL-1β给药也是如此。导致老年大鼠发烧的根本机制可能是周围与大脑之间的沟通不足。在老年大鼠中,外周细胞因子的作用可能会发生改变,从而使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-1β到达大脑以引起发烧,而较高的Ta会增加IL-1β流入大脑的能力,从而使老年大鼠发烧。将年轻的(3-5个月)和老的(23-29个月)Long-Evans大鼠在Ta 21或31°C下保持3天,然后静脉注射放射性标记的IL-1β以测量穿过血脑屏障的通道。幼鼠在两个Tas处有相似的IL-1β流入大脑,而老年鼠仅在Ta较热时才出现大量流入。这些数据表明,在凉爽的Ta时发烧不足可能是由于IL-1β进入脑部的流入减少所致。

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