Recent evidence has suggested that the carotid bodies might act as immunological sensors, detecting pro-inflammatory mediators and signalling to the central nervous system, which, in turn, orchestrates autonomic responses. Here, we confirmed that the TNF-α receptor type I is expressed in the carotid bodies of rats. The systemic administration of TNF-α increased carotid body afferent discharge and activated glutamatergic neurons in the nucleus tractus solitarius (NTS) that project to the rostral ventrolateral medulla (RVLM), where many pre-sympathetic neurons reside. The activation of these neurons was accompanied by an increase in splanchnic sympathetic nerve activity. Carotid body ablation blunted the TNF-α-induced activation of RVLM-projecting NTS neurons and the increase in splanchnic sympathetic nerve activity. Finally, plasma and spleen levels of cytokines after TNF-α administration were higher in rats subjected to either carotid body ablation or splanchnic sympathetic denervation. Collectively, our findings indicate that the carotid body detects circulating TNF-α to activate a counteracting sympathetic anti-inflammatory mechanism.

最近的证据表明，颈动脉体可能充当免疫传感器，检测促炎介质并向中枢神经系统发出信号，进而协调自主反应。在这里，我们证实了 I 型 TNF-α 受体在大鼠的颈动脉体中表达。TNF-α的全身给药增加了颈动脉体的传入放电，并激活了孤束核（NTS）中的谷氨酸能神经元，该神经元投射到延髓腹外侧（RVLM），许多前交感神经元所在的位置。这些神经元的激活伴随着内脏交感神经活动的增加。颈动脉体消融减弱了 TNF-α 诱导的 RVLM 投射 NTS 神经元的激活和内脏交感神经活动的增加。最后，在接受颈动脉体消融或内脏交感神经去神经支配的大鼠中，给予 TNF-α 后血浆和脾脏细胞因子水平较高。总的来说，我们的研究结果表明颈动脉体检测到循环的 TNF-α 以激活​​抵消交感神经抗炎机制。