TY - JOUR
T1 - Vagus-brain communication in atherosclerosis-related inflammation
T2 - A neuroimmunomodulation perspective of CAD
AU - Gidron, Yori
AU - Kupper, Nina
AU - Kwaijtaal, Martijn
AU - Winter, Jobst
AU - Denollet, Johan
N1 - Funding Information:
This work was supported by a VICI grant from the Netherlands Organisation for Scientific Research (NWO; grant no. 453-04-004).
PY - 2007/12/1
Y1 - 2007/12/1
N2 - The current understanding of the pathophysiology of atherosclerosis leading to coronary artery disease (CAD) emphasizes the role of inflammatory mediators. Given the bidirectional communication between the immune and central nervous systems, an important question is whether the brain can be "informed" about and modulate CAD-related inflammation. A candidate communicator and modulator is the vagus nerve. Until now, the vagus nerve has received attention in cardiology mainly due to its role in the parasympathetic cardiovascular response. However, the vagus nerve can also "inform" the brain about peripheral inflammation since its paraganglia have receptors for interleukin-1. Furthermore, its efferent branch has a local anti-inflammatory effect. These effects have not been considered in research on the vagus nerve in CAD or in vagus nerve stimulation trials in CAD. In addition, various behavioural interventions, including relaxation, may influence CAD prognosis by affecting vagal activity. Based on this converging evidence, we propose a neuroimmunomodulation approach to atherogenesis. In this model, the vagus nerve "informs" the brain about CAD-related cytokines; in turn, activation of the vagus (via vagus nerve stimulation, vagomimetic drugs or relaxation) induces an anti-inflammatory response that can slow down the chronic process of atherogenesis.
AB - The current understanding of the pathophysiology of atherosclerosis leading to coronary artery disease (CAD) emphasizes the role of inflammatory mediators. Given the bidirectional communication between the immune and central nervous systems, an important question is whether the brain can be "informed" about and modulate CAD-related inflammation. A candidate communicator and modulator is the vagus nerve. Until now, the vagus nerve has received attention in cardiology mainly due to its role in the parasympathetic cardiovascular response. However, the vagus nerve can also "inform" the brain about peripheral inflammation since its paraganglia have receptors for interleukin-1. Furthermore, its efferent branch has a local anti-inflammatory effect. These effects have not been considered in research on the vagus nerve in CAD or in vagus nerve stimulation trials in CAD. In addition, various behavioural interventions, including relaxation, may influence CAD prognosis by affecting vagal activity. Based on this converging evidence, we propose a neuroimmunomodulation approach to atherogenesis. In this model, the vagus nerve "informs" the brain about CAD-related cytokines; in turn, activation of the vagus (via vagus nerve stimulation, vagomimetic drugs or relaxation) induces an anti-inflammatory response that can slow down the chronic process of atherogenesis.
KW - Atherosclerosis
KW - Autonomic nervous system
KW - Coronary artery disease
KW - Inflammation
KW - Vagus nerve
UR - http://www.scopus.com/inward/record.url?scp=36049003122&partnerID=8YFLogxK
U2 - 10.1016/j.atherosclerosis.2006.10.009
DO - 10.1016/j.atherosclerosis.2006.10.009
M3 - Review article
C2 - 17101139
AN - SCOPUS:36049003122
SN - 0021-9150
VL - 195
SP - e1-e9
JO - Atherosclerosis
JF - Atherosclerosis
IS - 2
ER -