Bioelectronic stimulation of the celiac vagus nerve recapitulates Angiotensin II-induced splenic noradrenergic activation, promoting PlGF release and egress of CD8 effector T cells.
This study identifies a neuroimmune pathway where celiac vagus nerve stimulation mimics AngII-induced splenic noradrenergic activation, driving CD8 T cell egress.
Angiotensin II (AngII) is a peptide hormone that affects the cardiovascular system, not only through typical effects on the vasculature, kidneys, and heart, but also through less understood roles mediated by the brain and the immune system. Here, we address the hard-wired neural connections within the autonomic nervous system that modulate splenic immunity. Chronic AngII infusion triggers burst firing of the vagus nerve celiac efferent, an effect correlated with noradrenergic activation in the spleen and T cell egress. Bioelectronic stimulation of the celiac vagus nerve, in the absence of other challenges and independently from afferent signals to the brain, evokes the noradrenergic splenic pathway to promote release of a growth factor mediating neuroimmune crosstalk, placental growth factor (PlGF), and egress of CD8 effector T cells. Our findings also indicate that the neuroimmune interface mediated by PlGF and necessary for transducing the neural signal into an effective immune response is dependent on α-adrenergic receptor signaling.
Carnevale et al. (Tue,) reported a other. Celiac vagus nerve stimulation and Angiotensin II infusion was evaluated on Splenic noradrenergic activation and egress of CD8 effector T cells. Bioelectronic stimulation of the celiac vagus nerve recapitulates Angiotensin II-induced splenic noradrenergic activation, promoting PlGF release and egress of CD8 effector T cells.