VIP Peptide And Lung Research From Harlem And Beyond

January 30, 2024

Studies suggest that VIP may be useful as a research compound in the context of neurological illness, pulmonary fibrosis, inflammatory bowel disease, and cardiac fibrosis by potentially decreasing inflammation.

The peptide seems to be potentially efficacious in a variety of fibrotic pathways. Research suggests that it may give advantages in the common process of fibrosis that causes morbidity and death. It has been hypothesized that VIP is a possible immune system regulator with general anti-inflammatory and antifibrotic characteristics that seem to be mediated via anti-inflammatory activities. The peptide has been speculated to protect the central nervous system from injury, making it a prime target for study because of the importance placed on its potential to safeguard cognitive function in the face of neurodegenerative illness.

VIP Peptide: What is it?

VIP, also known as vasoactive intestinal polypeptide (PHM27), is a short peptide hormone produced in almost all vertebrates’ digestive tract, pancreas, and brain. VIP has been purported to bind to G protein-coupled receptors of the class II subtype. Other hypothesized properties that VIP peptide may have are:

  • It may boost the rate of glycogen breakdown in the liver and muscles.
  • It may reduce tension in the intestinal and gastric smooth muscles.
  • It may incite cardiac muscle contraction (by increasing both heart rate and contraction strength)
  • It may increase water retention via the digestive system.
  • It may control the production of prolactin.
  • It may protect cartilage.
  • It may prevent cell death caused by oxidative stress and ischemia.
  • It may influence the activity of autonomic nerves.
  • It may regulate circadian rhythm by using light signals to synchronize the central nervous system (particularly neurons in the suprachiasmatic nucleus).

VIP has always been intruiging for researchers for all the above hypotheses. With so much study on VIP, it would be hard to discuss its numerous elements in a single article. A few of the most salient aspects are highlighted here, most notably the theory that VIP may decrease inflammation and fibrosis in various organs.


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VIP Peptide and Inflammation

Research suggests that the immunological nerve fibers in the blood vessels of the central nervous system, peripheral nervous system, and heart are a major source of VIP. Additionally, VIP is purported to be generated directly by immune system cells, which might help stimulate Th2-type responses, possibly decreasing inflammation and calming the immune system. Extensive research has been done into VIP and its derivatives as possible inflammatory mediators in gastrointestinal illness, cardiovascular disease, and neuroinflammatory conditions.

VIP has been assumed to enhance intestinal barrier homeostasis and decrease inflammation caused by Th1 cell activities in the context of inflammatory bowel illnesses (IBDs) such as Crohn’s disease and ulcerative colitis. In particular, this latter strategy seems to induce T cells capable of generating interleukin-10, a peptide that suppresses inflammation. It has emerged in recent years that Th1 inflammation is a key mechanism in inflammatory bowel disease (IBD).

The effect intestinal barrier function should not be overstated since it contributes to inflammatory bowel disease etiology. In particular, more antigenic material in the intercellular space, where it is more likely to interact with immune cells and kick off an inflammatory response, is hypothesized to result from reduced barrier function. VIP seems to enhance barrier function by reducing antigen presentation to immune cells, which is thought to be an early stage in the development of colitis and severe inflammatory bowel disease.

VIP Peptide and Lung Activity

VIP has been theorized to affect lung function in at least two ways. As a first mechanism, VIP seems to regulate inflammation-induced pulmonary vascular remodeling. It appears to have this effect by reducing a peptide termed NFAT, which stimulates T cells and increases inflammation. VIP seems to regulate T-cell-mediated inflammation in the lungs, a function that has been challenging to study using existing models of inflammation. For example, inhibiting NFAT may be crucial in avoiding pulmonary fibrosis, the last step of many inflammatory diseases, including chronic obstructive pulmonary disease (COPD) and sarcoidosis.

VIP also appears to reduce the growth of pulmonary smooth muscles. The multiplication of smooth muscle cells is a chronic complication of lung inflammation exacerbated by bronchial asthma. Asthma causes chronic inflammation, and it is hoped that VIP may offer a way to lessen that inflammation.

The possible vasodilatory potential of VIP, which is already considered to support blood pressure regulation, may also have a particularly strong influence on pulmonary vasculature, as data suggests. Initial studies on VIP purport that it may increase cardiac output and improve venous oxygen saturation via lowering pulmonary artery blood pressure. While additional research is needed, there is optimism that VIP might provide a novel approach in the context of lung function in primary vascular diseases.

VIP Peptide and the Brain

VIP has been suggested to function as a neurotransmitter, a neurotroph/neurogenic, and an anti-inflammatory/neuroprotectant in the central nervous system. It has been speculated that VIP may function similarly in the central nervous system as in the intestinal mucosa. Here, the peptide was assumed to aid in keeping the blood-brain barrier (BBB) functioning normally. The BBB is a cellular barrier separating CNS tissue from the blood arteries. It governs everything from feeding and oxygenation to immune function by regulating what enters neural tissue. Compromise of the BBB has been implicated in the pathogenesis of multiple sclerosis, encephalomyelitis, and possibly stroke.

In addition to its alleged neuroprotective potential in Parkinson’s disease, VIP has been speculated to control beta-amyloid formation in animal models of Alzheimer’s disease. Data suggests that VIP might have a crucial role as a neuroprotectant in the developing brain, where it may protect against excitotoxic white matter injury and promote the myelination of neurons in the presence of fatty acids. Researchers suggest that VIP may be useful in the context of Parkinson’s disease by changing the immunological balance away from inflammatory Th1 responses and toward anti-inflammatory Th2 responses, as in other inflammatory conditions.

The precise function of VIP in AD is less certain. The brains of research models of Alzheimer’s disease have been indicated to have reduced amounts of the peptide VIP and its amino acid byproducts. Although the significance of VIP in the etiology of the illness is not yet fully understood, infusion of the peptide into the brains of mice appeared to significantly reduce beta-amyloid levels.

Researchers interested in further studying VIP peptides may find them for sale at Core Peptides, the highest-quality research peptides vendor available online.

References

[i] E. Gonzalez-Rey and M. Delgado, “Role of vasoactive intestinal peptide in inflammation and autoimmunity,” Curr. Opin. Investig. Drugs Lond. Engl. 2000, vol. 6, no. 11, pp. 1116–1123, Nov. 2005.

[ii] E. Gonzalez-Rey and M. Delgado, “Role of vasoactive intestinal peptide in inflammation and autoimmunity,” Curr. Opin. Investig. Drugs Lond. Engl. 2000, vol. 6, no. 11, pp. 1116–1123, Nov. 2005.

[iii] S. Seo et al., “Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis,” J. Pediatr. Surg., vol. 54, no. 12, pp. 2520–2523, Dec. 2019, doi: 10.1016/j.jpedsurg.2019.08.038.

[iv] E. Gonzalez-Rey and M. Delgado, “Therapeutic treatment of experimental colitis with regulatory dendritic cells generated with vasoactive intestinal peptide,” Gastroenterology, vol. 131, no. 6, pp. 1799–1811, Dec. 2006, doi: 10.1053/j.gastro.2006.10.023.

[v] S. I. Said, “The vasoactive intestinal peptide gene is a key modulator of pulmonary vascular remodeling and inflammation,” Ann. N. Y. Acad. Sci., vol. 1144, pp. 148–153, Nov. 2008, doi: 10.1196/annals.1418.014.

[vi] A. M. Szema et al., “NFATc3 and VIP in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary Disease,” PloS One, vol. 12, no. 1, p. e0170606, 2017, doi: 10.1371/journal.pone.0170606.

[vii] “Vasoactive Intestinal Peptide – an overview | ScienceDirect Topics.” https://www.sciencedirect.com/topics/neuroscience/vasoactive-intestinal-peptide

[viii] V. Petkov et al., “Vasoactive intestinal peptide as a new drug for treatment of primary pulmonary hypertension,” J. Clin. Invest., vol. 111, no. 9, pp. 1339–1346, May 2003, doi: 10.1172/JCI17500.

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