PT  - JOURNAL ARTICLE
AU  - Pedro L. Katayama
AU  - Isabela P. Leirão
AU  - Alexandre Kanashiro
AU  - João Paulo M. Luiz
AU  - Fernando Q. Cunha
AU  - Luiz C. C. Navegantes
AU  - Jose V. Menani
AU  - Daniel B. Zoccal
AU  - Débora S. A. Colombari
AU  - Eduardo Colombari
TI  - The Carotid Body Detects Circulating Tumor Necrosis Factor-Alpha to Activate a Sympathetic Anti-Inflammatory Reflex
AID  - 10.1101/2021.10.20.463417
DP  - 2021 Jan 01
TA  - bioRxiv
PG  - 2021.10.20.463417
4099  - http://biorxiv.org/content/early/2021/12/04/2021.10.20.463417.short
4100  - http://biorxiv.org/content/early/2021/12/04/2021.10.20.463417.full
AB  - 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 demonstrated 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 the majority of pre-sympathetic neurons reside. The activation of these neurons was accompanied by generalized activation of the sympathetic nervous system. 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.Competing Interest StatementThe authors have declared no competing interest.