vasoactive intestinal peptide/inflamație

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Signaling mechanisms of vasoactive intestinal peptide in inflammatory conditions.

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The vasoactive intestinal peptide (VIP) is a neuropeptide belonging to the secretin/glucagon family of peptides, which exerts a wide spectrum of immunological functions controlling the homeostasis of immune system through different receptors expressed in various immunocompetent cells. In the last

Dual bronchodilatory and pulmonary anti-inflammatory activity of RO5024118, a novel agonist at vasoactive intestinal peptide VPAC2 receptors.

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OBJECTIVE Vasoactive intestinal peptide is expressed in the respiratory tract and induces its effects via its receptors, VPAC(1) and VPAC(2). RO5024118 is a selective VPAC(2) receptor agonist derived via chemical modification of an earlier VPAC(2) agonist, RO0251553. In the present studies, we

Inhibitory effects of vasoactive intestinal peptide on superoxide anion formation by N-formyl-methionyl-leucyl-phenylalanine-activated inflammatory cells in vitro.

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Effects of vasoactive intestinal peptide (VIP) on superoxide anion (O2-) formation by N-formyl-methionyl-leucyl-phenylalanine (fMLP)-activated inflammatory cells from healthy volunteers were investigated using 2-methyl-6-[p-methoxyphenyl]-3,7-dihydroimidazo [1,2-a]pyrazin-3-one (MCLA) as a

Immunocytochemical localization of vasoactive intestinal peptide and substance P in the colon from normal subjects and patients with inflammatory bowel disease.

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Neuropeptides form a part of the brain-gut axis which may regulate gastrointestinal functions, including immune regulation. Various changes in the neuropeptides--most important, vasoactive intestinal peptide and substances P (VIP and SP)--have been described in inflammatory bowel disease. We

Vasoactive intestinal peptide overexpression mediated by lentivirus attenuates lipopolysaccharide-induced acute lung injury in mice by inhibiting inflammation.

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Vasoactive intestinal peptide (VIP) is one of the most abundant neuropeptides in the lungs with various biological characters. We have reported that VIP inhibited the expressions of TREM-1 and IL-17A, which are involved in the initiation and amplification of inflammation in acute lung injury (ALI).

Expression of mRNA for vasoactive intestinal peptide in normal human colon and during inflammation.

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The availability of colon provides a ready source of human neurons. Among the products of nerve cell bodies, vasoactive intestinal peptide is a neuropeptide that serves as a marker of non-adrenergic, non-cholinergic inhibitory nerves in colon. These nerves have been proposed to be involved in

Colonic vasoactive intestinal peptide nerves in inflammatory bowel disease.

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Vasoactive intestinal peptide is a neuropeptide with potent modulatory activity on intestinal immunity and may be implicated in the pathogenesis of inflammatory bowel disease (IBD). Previous studies have reported abnormal morphology of vasoactive intestinal peptide-stained enteric nerves, in

Substance P and vasoactive intestinal peptide in bullous and inflammatory skin disease.

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Immunoreactivity (IR) of substance P (SP) and Vasoactive Intestinal Peptide (VIP) were determined by radioimmunoassay in serum of 56 patients with inflammatory skin diseases, in blister fluid of 40 patients with spontaneous blisters and 31 subjects with induced skin blisters. Serum concentrations of

The vasoactive intestinal peptide gene is a key modulator of pulmonary vascular remodeling and inflammation.

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Pulmonary vascular remodeling and inflammation often coexist in clinical and experimentally induced pulmonary arterial hypertension (PAH). In some instances, the pulmonary hypertension may be the primary, or at least the initial, problem, while inflammatory or autoimmune responses appear to initiate

Role of vasoactive intestinal peptide and inflammatory mediators in enteric neuronal plasticity.

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Complex circuits involving both local intrinsic neurones (i.e. enteric nervous system; ENS) and extrinsic neurones achieve nervous control of digestive functions. The ENS is comprised of many functionally different types of neurons: sensory neurons, interneurons and secreto-motor neurons. Each

Calcitonin gene-related peptide II, substance P and vasoactive intestinal peptide in plasma and synovial fluid from patients with inflammatory joint disease.

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Immunoreactive plasma and synovial fluid concentrations of calcitonin gene-related peptide II (CGRP II), substance P and vasoactive intestinal peptide (VIP) were measured in patients with osteoarthritis, gout and rheumatoid arthritis. Significantly higher levels of CGRP II and substance P-like

Regional content of enteric substance P and vasoactive intestinal peptide during intestinal inflammation in the parasitized ferret.

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Our aim was to characterize and quantitate changes in two key neuropeptides, substance P (SP) and vasoactive intestinal peptide (VIP), that are involved in governing neurally-mediated gastrointestinal (GI) reflex activity during enteric inflammation in the ferret. Neuropeptide content was determined

Vasoactive intestinal peptide as a laboratory supplement to clinical activity index in inflammatory bowel disease.

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Circulating levels of vasoactive intestinal peptide (VIP) in plasma were measured in gauging activity in inflammatory bowel disease (IBD). One hundred-fifteen adult IBD patients were studied cross-sectionally and prospectively, 48 with ulcerative colitis (UC) and 67 with Crohn's disease (CD).

Vasoactive intestinal peptide reduces the inflammatory profile in mice infected with Trypanosoma cruzi.

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Vasoactive intestinal peptide (VIP) has gained great prominence because of its therapeutic potential, which is ascribed to its ability to regulate innate immunity, inhibit antigen-specific Th1 cell responses, and generate T regulatory cells. Additionally, VIP may act as a natural antimicrobial

Vasoactive intestinal peptide and inflammatory cytokines enhance vascular endothelial growth factor production from epidermal keratinocytes.

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BACKGROUND Overexpression of vascular endothelial growth factor (VEGF) in epidermal lesions of psoriasis is well documented; however, its underlying mechanisms are largely unknown. We have recently demonstrated that vasoactive intestinal peptide (VIP) induces the production of cytokines such as

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