The G Protein-Coupled Receptor, VPAC1, is The Principle Driver for VIP Deficiency-Induced Alterations of Gut Microbiota in C57BL/6 Mice.

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Abstract
Previous studies in our lab linked vasoactive intestinal peptide (VIP) signaling to gut microbiota stability. Although VIP-deficient mice demonstrated a gut microbiota dysbiosis characterized by a reduction in both the Firmicutes:Bacteroidetes phyla ratio and α-diversity, the mechanism for this observation was not known. To this end, we conducted a similar study analyzing fecal samples from VIP receptor-deficient mice, known as VPAC1 and VPAC2, by 16S rRNA sequencing. Samples from male and female wildtype (WT, n=30), heterozygous (HET, n=31) and homozygous mutant (KO, n=32) mice were analyzed. Our data revealed that genetic deletion of either receptor resulted in statistically significant changes in fecal β-diversity, with VPAC1 KO samples also demonstrating loss in bacterial α-diversity. Comparing 94 statistically altered OTUs from VPAC1 samples, more than 62% were similar to those found in VIP KO samples. We conclude that VIP→VPAC1 signaling is a major driving force regulating intestinal homeostasis and a stable gut microbiota.