Apical splenic nerve electrical stimulation discloses an anti-inflammatory pathway relying on adrenergic and nicotinic receptors in myeloid cells

Publication date: Available online 15 March 2019Source: Brain, Behavior, and ImmunityAuthor(s): Mélanie Guyot, Thomas Simon, Clara Panzolini, Franck Ceppo, Douglas Daoudlarian, Emilie Murris, Eric Macia, Sophie Abélanet, Arun Sridhar, Margriet J. Vervoordeldonk, Nicolas Glaichenhaus, Philippe BlancouAbstractThe autonomic nervous system innervates all lymphoid tissues including the spleen therefore providing a link between the central nervous system and the immune system. The only known mechanism of neural inhibition of inflammation in the spleen relies on the production of norepinephrine by splenic catecholaminergic fibers which binds to β2-adrenergic receptors (β 2-ARs) of CD4+ T cells. These CD4+ T cells trigger the release of acetylcholine that inhibits the secretion of inflammatory cytokines by macrophages through α7 nicotinic acetylcholine receptor (α7nAchRs) signaling. While the vagal anti-inflammatory pathway has been extensively studied in rodents, it remains to be determined whether it coexists with other neural pathways. Here, we have found that three nerve branches project to the spleen in mice. While two of these nerves are associated with an artery and contain catecholaminergic fibers, the third is located at the apex of the spleen and contain both catecholaminergic and cholinergic fibers. We found that electrical stimulation of the apical nerve, but not the arterial nerves, inhibited inflammation independently of lymphocytes. In striking contrast to the an...
Source: Brain, Behavior, and Immunity - Category: Neurology Source Type: research