VIP
VIP (vasoactive intestinal peptide) is an endogenous 28-amino-acid neuropeptide that signals through VPAC1/VPAC2 receptors to suppress inflammatory immune-cell activity and skew T-helper responses toward Th2, based largely on rodent and cell-culture research rather than human clinical outcome trials.
This page is a research-orientation summary, not a dosing guide. For anything beyond general background, read the primary literature or talk to a qualified clinician — specifics like amount, frequency, or administration aren't something we publish here.
What it does & how it works
VIP binds two G-protein-coupled receptors, VPAC1 and VPAC2 (both mainly Gαs-coupled to raise intracellular cAMP, with VPAC1 also coupling to Gαq/Ca2+ signaling). Through these receptors VIP suppresses macrophage- and dendritic-cell-driven inflammatory signaling, differentially regulates costimulatory molecule (CD80/CD86) expression on immature versus activated dendritic cells, and promotes T-helper-2 (Th2) polarization while inhibiting activation-induced cell death of Th2 effector cells (via downregulation of FasL), favoring survival of Th2 memory cells over Th1 responses.
Typical results seen in research
Rodent and cell-culture studies show VIP has anti-inflammatory, Th2-skewing effects relevant to models of sepsis, arthritis, colitis, and neuroinflammation, and VIP/PACAP signaling is implicated in maintaining blood-brain barrier integrity and modulating neuroinflammation in epilepsy models. Human data identified are largely limited to receptor-signaling characterization in isolated immune cells (e.g., T-cell lines) rather than clinical trials of administered VIP; the intranasal VIP protocols popularized for "chronic inflammatory response syndrome"/mold illness in some clinical practices are not supported by peer-reviewed clinical trial evidence that could be located.
How it’s commonly used
In research settings, VIP has been administered via intranasal, intravenous, or local injection routes in both animal models and isolated human cell studies. It is also used investigationally as an inhaled or intranasal formulation in some clinical research contexts, though this is not the same as an FDA-approved therapeutic use.
- Journal of Leukocyte Biology · 2004 VIP/PACAP oppositely affects immature and mature dendritic cell expression of CD80/CD86 and the stimulatory activity for CD4+ T cells
- Archives of Physiology and Biochemistry · 2001 VIP and PACAP enhance the in vivo generation of memory TH2 cells by inhibiting peripheral deletion of antigen-specific effectors
- Pharmacological Research · 2021 VIPergic neuroprotection in epileptogenesis: challenges and opportunities
Curated from published literature for research orientation. Not an exhaustive review, and not a substitute for reading primary sources.