Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system

Iwasaki, Mari; Akiba, Yasutada; Kaunitz, Jonathan D.

doi:10.12688/f1000research.18039.1

Cited by 123 publications

(112 citation statements)

References 120 publications

(168 reference statements)

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“…It was demonstrated that VIP plays a key role in the pathogenesis of inflammatory bowel syndrome (IBD) (Abad et al 2012). Infiltrates of immune cells and myofibroblasts VIP positive, have also been observed in the lamina propria as a response to the inflammatory state (Iwasaki et al 2019) (Figure 2). Immunofluorescence reactions of a-SMA (green signal) and VIP (red signal) confirmed immunoperoxidase method.…”

Section: Light Microscopy and Immunohistochemical Analysismentioning

confidence: 99%

“…VIP is also expressed by immune cells, such as T cells, B cells, mast cells, eosinophils (Pozo et al 2000). It stimulates the secretion of HCO 3 -ions, acts on smooth muscles and plays a role as an anti-inflammatory mediator, regulating the abundance of cytokines, also inducing differentiation from Th cell to Th2 (Iwasaki et al 2019). VIP also is an inhibitor of gastric juice and promotes intestinal motility (Soares et al 2015;Wu et al 2015).…”

Section: Light Microscopy and Immunohistochemical Analysismentioning

confidence: 99%

“…Vasoactive intestinal polypeptide (VIP) is among the most common neurotransmitter in the gut of vertebrates including fish (Olsson 2009;Zaccone et al 2015;Lauriano et al 2017). VIP is a "neuroimmunopeptide" localized in different regions of the gut as nerve cell bodies and fibers in submucosal and muscular layers (Costa and Furness 1983); it is also expressed in immune cells, such as activated T cells and B cells, mast cells, and eosinophils (Leceta et al 1994;Iwasaki et al 2019). VIP is involved in the pathogenesis of acute ethanol-induced gastric mucosal damage, resulting significantly increased in rats treated intragastrically with 1.0 ml 96% ethanol as compared with saline-treated animals (P < 0.05) (Karmeli et al 1993).…”

Section: Introductionmentioning

confidence: 99%

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Biological effect of astaxanthin on alcohol-induced gut damage in Carassius auratus used as experimental model

Alesci

Pergolizzi

Gervasi

et al. 2020

Natural Product Research

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Alcohol and its metabolites are responsible for damage both within the gastrointestinal tract and other organs. Alcohol abuse promote intestinal inflammation, that may be the cause of multiple organ dysfunctions and chronic disorders. In this research, the effect of astaxanthin, a powerful antioxidant with several biological effects, on alcohol damage-induced in the intestine of Carassius auratus, was investigated. In the fishes exposed to ethanol, an increase of the intestinal epithelium mucous cells and circulating macrophages, with intestinal mucosa disorganization was observed. In contrast, in the fishes treated with astaxanthin intestinal morphology was restored. By immunohistochemical analysis, using a-Smooth Muscle Actin (a-SMA) and Vasoactive intestinal polypeptide (VIP) antibodies, a reduction of inflammatory states alcohol-induced was evident, with more regular muscularis submucosa and more organized intestinal mucosa without inflammatory cells. The results suggest that astaxanthin treatments can be a good candidate for preventing damage within the gastrointestinal associated with excessive alcohol consumption.

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Section: Light Microscopy and Immunohistochemical Analysismentioning

confidence: 99%

Section: Light Microscopy and Immunohistochemical Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Biological effect of astaxanthin on alcohol-induced gut damage in Carassius auratus used as experimental model

Alesci

Pergolizzi

Gervasi

et al. 2020

Natural Product Research

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“…On the other hand, clinical and animal studies of intestinal permeability and vascular flow have not succeeded in identifying such mechanisms in cholera patients [ 21 ]. VIPergic pathways actually reduce epithelial paracellular permeability [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

“…Paradoxically, elevations of cAMP after CT [ 26 ] or forskolin [ 27 ] are also associated with increased absorption of substrates of the active transport of sodium, such as glucose and glycine, suggesting that all or part of the cAMP elevation (or alterations in cAMP isoform variants) might represent a compensatory mechanism, aimed at overcoming the absorptive defect exemplified by the failure of absorption of plain saline solutions seen in cholera patients [ 28 ]. The mechanisms by which cAMP and VIP produce their effects are highly complex and beyond the scope of this report, but have been detailed in recent publications [ 22 , 29 ].…”

Section: Introductionmentioning

confidence: 99%

Cholera and Pancreatic Cholera: Is VIP the Common Pathophysiologic Factor?

et al. 2020

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Background: Cholera remains a major global health problem, causing high output diarrhea leading to severe dehydration and shock in developing countries. We aimed to determine whether vasoactive intestinal polypeptide (VIP), the mediator of pancreatic cholera syndrome, has a role in the pathophysiology of human cholera. Methods: We conducted a prospective observational study of cholera cases hospitalized with severe dehydration. Plasma and stool water levels of VIP were measured just after admission, after complete rehydration (3–4 h), at 24 h post-rehydration and at discharge after diarrhea ceased. Results: In total, 23 cholera patients were examined between January and August 2018. The geometric mean of stool VIP (sVIP) and plasma VIP (pVIP) on admission were 207.67 and 8.34 pmol/L, respectively. pVIP values were all within the normal range (</= 30 pcmol/L); however, sVIP levels were very high at all timepoints, though less so just after rehydration. In multivariable GEE models, after adjustment for covariates, sVIP levels were significantly associated with duration of hospitalization (p = 0.026), total stool volume (p = 0.023) as well as stool output in the first 24 h (p = 0.013). Conclusions: The data suggest that VIP, which is released by intestinal nerves, may play an important role in human choleragenesis, and inhibitors of intestinal VIP merit testing for potential therapeutic benefits.

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Neuropeptides in Cancer: Friend and Foe?

Berisha

Borniger

2022

Advanced Biology

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highly dynamic network of various cell types (e.g., cancer cells, endothelial cells, immune cells, fibroblasts) that exert differential effects on neuronal activity within the local environment. Thus, complex signaling between cancer and stromal cells in the TME results in altered firing rates of local nerves. Reciprocally, increased neuronal activity and subsequent release of classical neurotransmitters and/or neuropeptides within the TME results in enhanced cancer progression and subsequent metastasis in various preclinical models and clinical studies. [5][6][7][8][9] Nerves interact with multiple stromal cells in the TME where they indirectly promote tumor growth, progression, and subsequent metastasis. [10] Several studies have demonstrated that sympathetic nerve innervation and subsequent release of the neurotransmitter norepinephrine (NE) is increased in breast tumors. [6,8,9] However, recent work has demonstrated that there is an inverse relationship between tumor weight and norepinephrine content (i.e., larger the size of the tumor, the lower the levels of NE), despite increased innervation of sympathetic nerves within the TME. [11] These findings may be attributed to a relatively unexplored phenomenon: neuropeptide release within the TME. Neuropeptides are molecular messengers that regulate a variety of functions in the central and peripheral nervous systems via binding G-protein-coupled receptors (GPCRs) on target cells. One of the many functions of neuropeptides is serving as growth factors for normal cells via the activation of the heterotrimeric G protein Gq and subsequent synthesis of second messengers and engagement of tyrosine phosphorylation cascades. Neuropeptides act as neuromodulators, in that they can alter the response of neurons to neurotransmitters and other circulating signals, such as leptin, ghrelin, glucose, and insulin-all of which are affected during cancer progression. [12][13][14][15][16][17] For example, both neuropeptide Y (NPY) and hypocretin/orexin neurons appear to mediate some of the orexigenic effects of centrally administered ghrelin as administration of NPY receptor antagonists attenuated ghrelininduced feeding. Similarly, ghrelin-induced feeding was suppressed in orexin knockout mice, indicating that ghrelin may stimulate feeding through both the orexin and NPY systems. [18] However, neuropeptide signaling is exploited within cancer cells and many studies demonstrate the contribution of neuropeptides in tumor cell proliferation and migration, [19] with many major neuropeptides also potentially contributing to cancer processes (see Table 1). Additionally, neuropeptides exert direct Neuropeptides are small regulatory molecules found throughout the body, most notably in the nervous, cardiovascular, and gastrointestinal systems. They serve as neurotransmitters or hormones in the regulation of diverse physiological processes. Cancer cells escape normal growth control mechanisms by altering their expression of growth factors, receptors, or intracellular signals, and neuropeptid...

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Recent advances in vasoactive intestinal peptide physiology and pathophysiology: focus on the gastrointestinal system

Cited by 123 publications

References 120 publications

Biological effect of astaxanthin on alcohol-induced gut damage in Carassius auratus used as experimental model

Biological effect of astaxanthin on alcohol-induced gut damage in Carassius auratus used as experimental model

Cholera and Pancreatic Cholera: Is VIP the Common Pathophysiologic Factor?

Neuropeptides in Cancer: Friend and Foe?

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