Prenatal fever could result in brain function impairments in the offspring. The present study investigated the effect of interleukin-6 (IL-6)-induced maternal fever on the offspring and the involvement of connexin 36 in this process. Pregnant C57BL/6J mice were injected with IL-6 on gestational day 15. The levels of iNOS and COX-2 were measured as an index of neuroinflammation in the brain of newborn pups. Offspring were treated with the connexin 36 (Cx36) inhibitor mefloquine at postnatal day (P)1-P3 or at P40-P42. Rotarod, grip traction, and foot fault tests were carried out to evaluate the motor behavior of adult offspring. Injection of IL-6 led to an elevation of the core temperature in the pregnant dams. Offspring of these dams showed significantly increased COX-2 and iNOS mRNA expression and protein levels in the whole-brain samples and significantly increased Cx36 in the cerebellum. Moreover, offspring of these dams showed motor deficits at an adult age. Neonatal administration of the Cx36 inhibitor mefloquine could prevent these motor deficits. Maternal fever during pregnancy induced by IL-6 injection could lead to neuroinflammation and motor deficits in the offspring. Neonatal inhibition of Cx36 could ameliorate the motor deficits in the offspring, indicating an involvement of Cx36 in the IL-6-induced maternal fever.

中文翻译：

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新生儿抑制 Connexin 36 可改善小鼠母体非感染性发热引起的胎儿脑损伤。


产前发烧可能会导致后代大脑功能受损。本研究调查了白细胞介素 6 (IL-6) 诱导的母体发热对后代的影响以及连接蛋白 36 在此过程中的参与。怀孕的 C57BL/6J 小鼠在妊娠第 15 天注射 IL-6。测量 iNOS 和 COX-2 的水平作为新生幼鼠大脑中神经炎症的指标。后代在出生后 (P)1-P3 或 P40-P42 时接受连接蛋白 36 (Cx36) 抑制剂甲氟喹治疗。进行旋转棒、握力牵引和足部故障测试来评估成年后代的运动行为。注射IL-6导致怀孕母鼠的核心温度升高。这些母鼠的后代全脑样本中 COX-2 和 iNOS mRNA 表达和蛋白质水平显着增加，小脑中 Cx36 显着增加。此外，这些水坝的后代在成年后表现出运动缺陷。新生儿服用 Cx36 抑制剂甲氟喹可以预防这些运动缺陷。怀孕期间注射 IL-6 引起的母亲发烧可能会导致后代的神经炎症和运动缺陷。新生儿抑制 Cx36 可以改善后代的运动缺陷，表明 Cx36 参与了 IL-6 诱导的母体发热。