The effect of vasoactive intestinal peptide (VIP) on mast cell invasion/degranulation in testicular interstitium of immobilized + cold stressed and β-endorphin-treated rats

Tunçel, Neşe; Gürer, Fi̇rdevs; Aral, Erinc; Uzuner, Kubi̇lay; Aydın, Yasemin; Bayçu, Cengiz

doi:10.1016/0196-9781(96)00083-6

Cited by 14 publications

(12 citation statements)

References 27 publications

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“…Vasoactive intestinal peptide (VIP) presents a number of features that offer promise for its potential usefulness in the management of cold‐restraint induced gastric ulcers. VIP relaxes vascular and non vascular smooth muscle, 16,17 inhibits mast cell degranulation, 18‐20 protects the tissues against oxygen free radical injury, and counteracts the response of inflammatory mediators. 21‐23…”

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confidence: 99%

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The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Tunçel

Erkasap

Şahıntürk

et al. 1998

Annals of the New York Academy of Sciences

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The pathogenesis of cold-restraint stress ulcer involves various factors and is not completely understood. Mast cell degranulation, increased gastric muscular contractility, diminished mucosal blood flow, release of several biogenic amines, activated polymorphonuclear leukocytes, and lipid peroxidation which results from toxic oxygen molecules were suggested to be related to the production of gastric damage by cold-restraint stress. Recent evidence strongly indicates that VIP has a modulatory effect on tissue injury. Sprague-Dawley rats were used in two series of experiments. One set of rats was exposed to cold-restraint stress with some of the rats pretreated with VIP. The second set of rats was exposed to cold-restraint stress and then was administered VIP for different durations. Cold-restraint stress induced gastric lesions and mast cell degranulation and also increased lipid peroxidation in gastric tissue. VIP prevented stress-induced ulcers and mast cell degranulation and protected gastric tissue from lipid peroxidation. When VIP was used after induction of stress ulcer it was therapeutically beneficial. Thanks to its antioxidant and anti-inflammatory activity, VIP can be valuable in the prevention of gastric mucosal damage induced by cold-restraint stress.

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confidence: 99%

“…25‐27 In addition to experimental hemorrhagic shock model, VIP also inhibits mast cell degranulation and proliferation and decreases histamine level in testicular tissue of rats exposed to cold‐restraint stress. 18,28…”

mentioning

confidence: 99%

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Tunçel

Erkasap

Şahıntürk

et al. 1998

Annals of the New York Academy of Sciences

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“…Collectively, these findings (3-8), Davidoff and colleagues' data (1 and Refs therein) and the recent results about Leydig cellimmune cell interactions (9)(10)(11)(12)(13)(14)(15)(16) suggest that a local neuroendocrine-immune link may exist within the testis. The Leydig cell-macrophage interaction in rodent testis was described (10)(11)(12), suggesting a role of testicular macrophages in both regulation of Leydig cell functions and promotion of Leydig cell development.…”

Section: See Review On Page 11mentioning

confidence: 73%

“…Indeed, Leydig cell express and/or secrete regulatory modules (1,4,6,9), with both activating and inhibitory effects on testicular immune cells. For example, the Leydig cellderived substance P, vasoactive intestinal polypeptide and (3endorphin (1) may affect mast cell activity (16,17) and T cell proliferation (6,8). Recently we observed mast cell increase in the heart after suppressing the Leydig cells by estrogen treat-ment of newborn rats indicating that Leydig cells also influence extratesticular immunocytes via negative endocrine way (15).…”

Section: See Review On Page 11mentioning

confidence: 99%

Leydig cell-immune cell interaction: an example of neuroendocrine-immune communication in testis

et al. 1996

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“…In this sense, previous studies showed that VIP protects tissues from the injury of ischemia-reperfusion, lipid peroxidation, and oxidant stress by inhibiting mast cell degranulation [179][180][181]. Recently, it was described that VIP inhibits mast cell degranulation and proliferation and also changes the granular content of mast cells [181][182][183][184]. According to these results, it was suggested that the downregulatory effect of VIP on the production of several proinflammatory cytokines might be via inhibition of the mast cellgranulocytes-cytokine cascade by modulation of mast cell activity.…”

Section: Preventive Effect Of Vip/pacap On Septic Shockmentioning

confidence: 93%

Therapeutical Approaches of Vasoactive Intestinal Peptide as a Pleiotropic Immunomodulator

González‐Rey¹,

Varela²,

Chorny³

et al. 2007

CPD

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The vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP) are two neuropeptides belonging to the VIP/secretin/glucagon family of peptides. VIP/PACAP are present and released from both innervation and immune cells, particularly Th2 cells, and exert a wide spectrum of immunological functions controlling the homeostasis of immune system through different receptors expressed in various immunocompetent cells. VIP/PACAP have a general anti-inflammatory effect, both in innate and adaptive immunity. In innate immunity, VIP/PACAP inhibit the production of pro-inflammatory cytokines and chemokines from macrophages, microglia and dendritic cells. In addition, VIP/PACAP reduce the expression of costimulatory molecules (particularly CD80 and CD86) on the antigen-presenting cells, and therefore reduce stimulation of antigen-specific CD4(+) T cells. In terms of adaptive immunity, VIP/PACAP promote Th2-type responses, and reduce the pro-inflammatory Th1-type responses. Several of the molecular mechanisms involved in the inhibition of cytokine and chemokine expression, and in the preferential development and/or survival of Th2 effectors, are perfectly known. Therefore, VIP/PACAP and analogues have been recently proposed as very promising candidates, alternative to other existing treatments, for treating acute and chronic inflammatory and autoimmune diseases, such as septic shock, rheumatoid arthritis, multiple sclerosis, Parkinson's disease, Crohn disease, or autoimmune diabetes. The aim of this review is firstly to update our knowledge of the cellular and molecular events relevant to VIP function on the immune system; and secondly to gather together recent data that support its role as a type 2 cytokine. Recognition of the central functions VIP plays in cellular processes is focusing our attention on this "very important peptide" as an exciting new candidate for therapeutic intervention and drug development.

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The effect of vasoactive intestinal peptide (VIP) on mast cell invasion/degranulation in testicular interstitium of immobilized + cold stressed and β-endorphin-treated rats

Cited by 14 publications

References 27 publications

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

The Protective Effect of Vasoactive Intestinal Peptide (VIP) on Stress‐Induced Gastric Ulceration in Rats

Leydig cell-immune cell interaction: an example of neuroendocrine-immune communication in testis

Therapeutical Approaches of Vasoactive Intestinal Peptide as a Pleiotropic Immunomodulator

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