Bassi, Gabriel S.
Castania, Jaci A.
Cunha, Thiago M.
Cunha, Fernando Q.
Martins Dias, Daniel P.
Salgado, Helio C.
Total Authors: 10
 Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Immunol, BR-14049900 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Med Sch Ribeirao Preto, Dept Pharmacol, BR-14049900 Ribeirao Preto, SP - Brazil
 Rutgers State Univ, New Jersey Med Sch, Newark, NJ 07103 - USA
Total Affiliations: 4
BRAIN BEHAVIOR AND IMMUNITY;
Web of Science Citations:
The baroreflex is a critical physiological mechanism controlling cardiovascular function by modulating both the sympathetic and parasympathetic activities. Here, we report that electrical activation of the baroreflex attenuates joint inflammation in experimental arthritis induced by the administration of zymosan into the femorotibial cavity. Baroreflex activation combined with lumbar sympathectomy, adrenalectomy, celiac subdiaphragmatic vagotomy or splenectomy dissected the mechanisms involved in the inflammatory modulation, highlighting the role played by sympathetic inhibition in the attenuation of joint inflammation. From the immunological standpoint, baroreflex activation attenuates neutrophil migration and the synovial levels of inflammatory cytokines including TNF, and IL-1 beta, but does not affect the levels of the anti-inflammatory cytokine IL-10. The anti-inflammatory effects of the baroreflex system are not mediated by IL-10, the vagus nerve, adrenal glands or the spleen, but by the inhibition of the sympathetic drive to the knee. These results reveal a novel physiological neuronal network controlling peripheral local inflammation. (C) 2015 Elsevier Inc. All rights reserved. (AU)