The carotid body detects circulating tumor necrosis factor-alpha to activate a sympathetic anti-inflammatory reflex

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-alpha receptor type I is expressed in the carotid bodies of rats. The systemic administration of TNF-alpha 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-alpha-induced activation of RVLM-projecting NTS neurons and the increase in splanchnic sympathetic nerve activity. Finally, plasma and spleen levels of cytokines after TNF-alpha administration were higher in rats subjected to either carotid body ablation or splanchnic sympa-thetic denervation. Collectively, our findings indicate that the carotid body detects circulating TNF-alpha to activate a counteracting sympathetic anti-inflammatory mechanism.

Automated summary

Recent evidence suggests that the carotid bodies act as immunological sensors, detecting pro-inflammatory mediators and signaling to the central nervous system to orchestrate autonomic responses. Carotid body ablation or splanchnic sympathetic denervation reduces the activation of neurons and sympathetic nerve activity induced by TNF-alpha, while increasing cytokine levels.