The splanchnic anti-inflammatory pathway, the efferent arm of the endogenous inflammatory reflex, has been shown to suppress the acute inflammatory response of rats to systemic lipopolysaccharide (LPS). Here we show for the first time that this applies also to mice, and that the reflex may be engaged by a range of inflammatory stimuli. Experiments were performed on mice under deep anaesthesia. Half the animals were subjected to bilateral section of the splanchnic sympathetic nerves, to disconnect the splanchnic anti-inflammatory pathway, while the remainder underwent a sham operation. Mice were then challenged intravenously with one of three inflammatory stimuli: the toll-like receptor (TLR)-4 agonist, LPS (60µg/kg), the TLR-3 agonist Polyinosinic:polycytidylic acid (Poly I:C, 1 mg/kg) or the TLR-2 and -6 agonist dipalmitoyl-S-glyceryl cysteine (Pam2cys, 34µg/kg). Ninety minutes later, blood was sampled by cardiac puncture for serum cytokine analysis. The splanchnic anti-inflammatory reflex action was assessed by comparing cytokine levels between animals with cut versus those with intact splanchnic nerves. A consistent pattern emerged: Tumor necrosis factor (TNF) levels in response to all three challenges were raised by prior splanchnic nerve section, while levels of the anti-inflammatory cytokine interleukin 10 (IL-10) were reduced. The raised TNF:IL-10 ratio after splanchnic nerve section indicates an enhanced inflammatory state when the reflex is disabled. These findings show for the first time that the inflammatory reflex drives a coordinated anti-inflammatory action also in mice, and demonstrate that its anti-inflammatory action is engaged, in similar fashion, by inflammatory stimuli mimicking a range of bacterial and viral infections.

内脏抗炎通路是内源性炎症反射的传出臂，已被证明可以抑制大鼠对全身性脂多糖 (LPS) 的急性炎症反应。在这里，我们首次表明这也适用于小鼠，并且反射可能会受到一系列炎症刺激的影响。在深度麻醉下对小鼠进行实验。一半的动物接受双侧内脏交感神经切片，以断开内脏抗炎通路，而其余动物则进行假手术。然后用三种炎症刺激物中的一种对小鼠进行静脉注射：toll 样受体 (TLR)-4 激动剂 LPS (60µg/kg)、TLR-3 激动剂 Polyinosinic:polycytidylic acid (Poly I:C, 1 mg/kg) 或 TLR-2 和 -6 激动剂二棕榈酰-S-甘油基半胱氨酸（Pam2cys，34μg/kg）。九十分钟后，通过心脏穿刺采集血液用于血清细胞因子分析。通过比较具有切割的动物之间的细胞因子水平来评估内脏抗炎反射作用。与内脏神经完整的人相比。出现了一致的模式：响应所有三种挑战的肿瘤坏死因子 (TNF) 水平因先前的内脏神经切片而升高，而抗炎细胞因子白细胞介素 10 (IL-10) 的水平降低。内脏神经切片后 TNF:IL-10 比率升高表明当反射被禁用时炎症状态增强。这些发现首次表明，炎症反射也在小鼠中驱动协调的抗炎作用，并证明其抗炎作用是通过模拟一系列细菌和病毒感染的炎症刺激以类似方式参与的。