Abstract| Volume 177, ISSUE 1, P43, August 2013

The vagus nerve: A modulator of intestinal inflammation

      Functional alterations in the central and the autonomic nervous system (i.e. depressions, decrease of the parasympathetic activity) have been described previously in patients with inflammatory bowel diseases (IBD). The cholinergic anti-inflammatory pathway is an efferent vagus nerve-(VN) based mechanism that regulates immune responses and cytokine production through α7nicotinic-acetylcholinereceptor (α7nAChR) signaling. Over the last 10 years, it has been described that the VN plays a tonic inhibitory role on inflammation and that pre-existing depression increases the development of experimental colitis via a deactivation of the VN. Tricyclic antidepressants prevent this deleterious effect. Moreover, electrical stimulation of the VN diminishes the production of inflammatory cytokines in colitis and endotoxemia. Despite its clinical implications, the precise physiological mechanisms contributing to the anti-inflammatory potential of the VN, remains unknown. Acetylcholine (Ach) is the principal neurotransmitter of the VN and previous studies analyzed the potential of cholinergic agonist to prevent TNF-α production in peritoneal macrophages, suggesting a direct link between the VN and the antigen presenting cell (APC)s. Recently, new data established the spleen as a key element in this anti-inflammatory effect, postulating that the VN stimulation induces Ach released by T cells, which inhibits cytokine production through the α7nAchR located on macrophages and splenocytes. Therefore, it is very likely other type of APCs, like dendritic cells (DC), play an important role in immune activation. Recent data demonstrated that pharmacological central cholinergic activation induced by the acetylcholinesterase inhibitor galantamine or a muscarinic acetylcholine receptor agonist treatments result in reduced mucosal inflammation associated with decreased pro-inflammatory cytokine secretion by splenic dendritic cells, mediated by α7nAChR signaling. Identification of the cellular mechanism underlying the protective role of VN may lead to novel therapeutic targets in the context of intestinal inflammation.
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