Vasoactive intestinal peptide (VIP, vasoactive intestinal polypeptide, PHM27) is a short peptide hormone endogenously produced in the gut, pancreas, and brain of most vertebrate animals. Researchers have suggested that the peptide may exhibit potential to control inflammation, particularly in the cases of neurodegenerative disease, pulmonary fibrosis, inflammatory bowel disease, and cardiac fibrosis. VIP has been suggested to act as an immune system regulator and has been classified by scientists as an anti-inflammatory peptide. It is of active scientific interest for its proposed ability to support cognitive function in the setting of neurodegenerative disease. VIP has been hypothesized to bind to class II G protein-coupled receptors.
OTHER KNOWN TITLES: PHM27, Vasoactive intestinal polypeptide
SEQUENCE: HSDAVFTDNYXRLRKQMAVKKYLNSXLN
MOLECULAR FORMULA: C147H237N43O43S
MOLECULAR WEIGHT: 3326.8 g/mol
VASOACTIVE INTESTINAL PEPTIDE (VIP) AND BOWEL INFLAMMATION
VIP is synthesized from the immune nerve fibers in blood vessels of the central and peripheral nervous systems and immune cells. It appears to reduce inflammation, as posited by research into inflammatory bowel diseases like Crohn’s and ulcerative colitis, by suppressing the production of interleukin-10 and improving intestinal barrier function.[1] Researchers report that “VIP and its analogs have been proposed as promising alternative candidates to existing [research] for … acute and chronic inflammatory and autoimmune diseases.” Compromised barrier function leads to increased antigenic material in the space between cells, which interacts with immune cells to trigger an inflammatory response. Studies have suggested that VIP may reduce the antigen presentation to immune cells by improving the barrier function.[2]
VASOACTIVE INTESTINAL PEPTIDE (VIP) AND LUNG FUNCTION
VIP appears to impact lung function through the following two pathways. The first mechanism alters pulmonary vascular remodeling in response to inflammation by suppressing a peptide called NFAT, which is suggested to activate T cells, leading to increased inflammation.[3] The scientists note that “VIP would emerge as an endogenous modulator of pulmonary vascular remodeling and inflammation, through its suppression of NFAT activation.” In particular, NFAT suppression may play an important role in preventing pulmonary fibrosis, the end stage of diverse inflammatory conditions such as COPD, sarcoidosis, etc. Smooth muscle cell proliferation is one of the long-term consequences of lung inflammation and is a challenge in bronchial asthma that has been uncontrolled for extended periods. VIP is a potential molecule that inhibits smooth muscle proliferation. Preliminary research also suggests that VIP may lower blood pressure in the pulmonary artery, leading to increased cardiac output and improved venous oxygen saturation.[4]
VASOACTIVE INTESTINAL PEPTIDE (VIP) AND TRANSPLANTS
Rejection by immune systems is one of the primary challenges faced in organ transplants. Currently, it is addressed through the use of broad-spectrum anti-inflammatory compounds. Unfortunately, these may lead to susceptibility to infection and ancillary actions, such as scarring and organ fibrosis. Researchers suggest that VIP may affect dendritic cells (DCs). By reducing DC proliferation and activation, VIP may help suppress immune responses, selectively inhibiting the proliferation of DCs that might cause an autoimmune reaction.[5]
VASOACTIVE INTESTINAL PEPTIDE (VIP) AND NEUROPROTECTION
Researchers propose that VIP may hold a three-fold role in the central nervous system: as neurotransmitter, neurotrophic/neurogenic, and anti-inflammatory/neuroprotectant. In research studies related to neuroprotection, the peptide may help maintain the very critical function of the blood-brain barrier (BBB). Compromise of the BBB has been implicated in multiple sclerosis, encephalomyelitis, and even stroke. VIP may offer neuroprotective functions in Alzheimer’s disease and Parkinson’s disease, and is being researched for its potential in this area. VIP appears to act as a possible neuroprotectant in the developing brain, warding off excitotoxic white matter damage and improving neuron fatty acid myelination.[6] The exact role of VIP in Alzheimer’s disease (AD) is less studied. Research suggests that the processing of VIP is inhibited in AD, with levels of the peptide and amino acid byproducts being lower in the brains of people affected by AD. The effect of VIP appears to be mediated through VPAC1 and VPAC2 receptors. In both cases, stimulation results in increased secretion of neurotrophic factors like ADNP (activity-dependent neurotrophic factor) and BDNF (brain-derived neurotrophic factor).[7] The peptide may help to protect synapses and astrocytes in these cases.
VASOACTIVE INTESTINAL PEPTIDE (VIP) AND CARDIAC FIBROSIS
As with lung disease, fibrosis is the end stage of several cardiac conditions. Cardiac fibrosis leads to several serious problems, including valve dysfunction, decreases in contractility, changes in cardiac filling, and more. As in lung disease, cardiac fibrosis is the common end-stage of many heart conditions, thus requiring a transplant. Research on rat models suggests that VIP may not only slow fibrosis down but may also reverse scarring. This possible effect is apparently partly mediated by a massive reduction in the expression of angiotensinogen and angiotensin receptor type 1a. This hypothosis seems plausible as angiotensin receptor blockers and ACE inhibitors have long been studied for their potential to slow down cardiac modeling/fibrosis and researchers suggest they are first line of prevention for fibrosis.[8]
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