Thermoregulation in patients suffering from multiple sclerosis (MS) is impaired and may result in either increases or decreases in body temperature. We have found that rat experimental autoimmune encephalitis (EAE), being a model of MS, is associated with body temperature disturbances as well. The purpose of the current study was to examine whether the altered body temperature in EAE-induced rats is due to either a deficit in thermoregulation or a controlled change in its set point. Subcutaneous injection of encephalitogenic emulsion into both pads of hind feet of the Lewis rats provoked EAE symptoms. Body temperature (Tb) of 6 rats was measured using biotelemetry system, and ambient temperature (Ta) preferred by 6 rats of another group was analyzed using thermal gradient system. Symptoms of EAE started 11 days postinjection and progressed quickly, culminating in a complete paralysis in rats placed in the gradient, which was associated with behavioural fever (accordingly, selected Ta raised to as much as 32.8 ± 0.5 °C vs 27.2 ± 0.6 °C in control rats). On the other hand, EAE rats, placed at a constant Ta of 24 °C, were able to generate fever (Tb of 37.8 ± 0.1 °C) at the start of the illness and then paralysis compromised fever (most likely due to an impairment of thermogenesis), which, surprisingly, resulted in recovery. We conclude that EAE onset in rats is associated with fever and its behavioural supporting leads to aggravation of the autoimmune neurotoxicity.

中文翻译：

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Lewis大鼠实验性自身免疫性脑炎的体温调节失衡

多发性硬化症 (MS) 患者的体温调节受损，可能导致体温升高或降低。我们发现，作为 MS 模型的大鼠实验性自身免疫性脑炎 (EAE) 也与体温紊乱有关。当前研究的目的是检查 EAE 诱导大鼠的体温变化是否是由于体温调节缺陷或其设定点的受控变化。将致脑炎乳液皮下注射到 Lewis 大鼠后足的两个脚垫中会引起 EAE 症状。使用生物遥测系统测量6只大鼠的体温(Tb)，使用热梯度系统分析另一组6只大鼠偏好的环境温度(Ta)。EAE 的症状在注射后 11 天开始并迅速进展，最终导致放置在梯度中的大鼠完全瘫痪，这与行为发热有关（因此，选定的 Ta 升高至 32.8 ± 0.5 °C，而对照大鼠为 27.2 ± 0.6 °C）。另一方面，将 EAE 大鼠置于 24 °C 的恒定温度下，能够在疾病开始时发热（Tb 为 37.8 ± 0.1 °C），然后麻痹导致发热（很可能是由于损伤所致）产热），令人惊讶的是，这导致了恢复。我们得出结论，大鼠的 EAE 发作与发烧有关，其行为支持导致自身免疫性神经毒性的加重。将 EAE 大鼠置于 24 °C 的恒定 Ta 温度下，能够在疾病开始时发热（Tb 为 37.8 ± 0.1 °C），然后瘫痪导致发热（很可能是由于产热受损），这，令人惊讶的是，导致恢复。我们得出结论，大鼠的 EAE 发作与发烧有关，其行为支持导致自身免疫性神经毒性的加重。将 EAE 大鼠置于 24 °C 的恒定 Ta 温度下，能够在疾病开始时发热（Tb 为 37.8 ± 0.1 °C），然后麻痹导致发热（很可能是由于产热受损），这，令人惊讶的是，导致恢复。我们得出结论，大鼠的 EAE 发作与发烧有关，其行为支持导致自身免疫性神经毒性的加重。