Abstract
Vasoactive intestinal peptide (VIP) is a potent immune regulator and secretagogue delivered by the peripheral nervous system to immune organs. VIP inhibits pro‐inflammatory, but increases anti‐inflammatory, cytokine secretion, deactivates macrophages and induces regulatory T cells. However, little is known about how VIP affects resting immune cells. Our laboratory discovered that VIP upregulated synaptotagmin (syt) XIII in resting CD4 T cells. Syt XIII is a calcium‐independent transmembrane protein that plays a vital role in vesicle exocytosis. This research is significant as the upregulation of syt XIII by VIP would maintain an important “exocytosis program” in resting immune cells. We hypothesize that VIP induced upregulation of syt XIII is dependent on its receptor VIP1, but not VIP2, through a Gαs→AC→PKA signaling mechanism in splenocytes. This research will utilize primary mouse splenocytes treated +/‐ VIP to identify peak expression of syt XIII by qPCR and western analysis. Optimal conditions will be repeated with VIP2 KO animals, VIP1 receptor antagonists and small molecule inhibitors of PKA (H89) and assessed by qPCR and/or western analysis for syt XIII expression. The significance of the proposed research is to better delineate how the nervous system regulates immunity.Grant Funding Source: This research will be supported by NIH/NIAID (R15 to GD).
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