Presentation: 2025 ND EPSCoR Annual conference
October 21, 2025, NDSU Memorial Union, Fargo, North Dakota
Impact of VIP Receptor Deficiency on Gut Barrier Integrity and Immune Cell Regulation
Teala
Matiur
Master's Student
North Dakota State University
Co-authors: Razia Dawlaty, Doctoral Student, North Dakota State University., Savanah Klegon, Doctoral Student, North Dakota State University., Joshua Eberts, Undergraduate, North Dakota State University., Kaley Quam, Undergraduate, North Dakota State University., Glenn Dorsam, Professor, North Dakota State University
Session
Poster number: 7
Ballroom
Vasoactive Intestinal Peptide (VIP) is a key neuroimmune regulator that maintains gut homeostasis by supporting epithelial integrity and balancing immune cell responses. VIP’s anti-inflammatory effects are primarily mediated through the VPAC1 receptor, a G-protein coupled receptor (GPCR). Disruptions in VIP signaling have been associated with inflammatory bowel disease (IBD) and heightened susceptibility to gut inflammation. While VIP’s role in modulating immune activity is established, its effects on intestinal epithelial cells (IECs) and lamina propria lymphocytes (LPLs) remain poorly defined. This study investigates how epithelial VIP→VPAC1 signaling contributes to homeostasis by measuring epithelial and immune cell frequencies. To achieve this, VPAC1 floxed mice were crossed with Villin-Cre hemizygous mice to generate gut epithelial conditional knockouts. At 8 weeks of age, small intestines were harvested, and epithelial and lamina propria immune cells were analyzed by flow cytometry. Lamina propria lymphocytes were profiled using CD45, CD127, a FITC-conjugated lineage dump, and viability dye. Intestinal epithelial cells were distinguished with EpCAM and CD45 exclusion, with additional epithelial markers currently being optimized. We anticipate that VIP deficiency may compromise epithelial integrity and disrupt mucosal immune regulation. Ongoing analyses will determine whether specific epithelial lineages and lymphocyte subsets, such as ILCs, Tregs, and eosinophils, are differentially affected. By clarifying VIP’s contribution to gut epithelial and immune balance, this study aims to identify novel roles for VPAC1 signaling in gut inflammation and highlight potential therapeutic targets for IBD and related disorders.