vasoactive-intestinal-peptide and Gastritis

Topics: Digestion; Esophageal Achalasia; Esophagitis, Peptic; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastritis; Glucagon; Humans; Ileum; Islets of Langerhans; Jejunum; Kidney Failure, Chronic; Liver; Protein Hydrolysates; Pyloric Antrum; Somatostatin; Vagotomy; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

To investigate the roles of the neuropeptides vasoactive intestinal peptide (VIP), substance P (SP), and calcitonin gene-related peptide (CGRP) in chronic gastritis and duodenitis in children.. Biopsy samples from the gastric and duodenal mucosa of 52 patients and 30 control subjects were obtained. Samples were taken for pathological examination, immunohistochemical staining, enzyme activity measurements and quantitative measurements of tissue peptide levels.. We observed differential effects of the disease on peptide levels, which were somewhat different from previously reported changes in chronic gastritis in adults. Specifically, SP was increased and CGRP and VIP were decreased in patients with gastritis. The changes were more prominent at sites where gastritis was severe, but significant changes were also observed in neighboring areas where gastritis was less severe. Furthermore, the degree of changes was correlated with the pathological grade of the disease. The expression of CD10, the enzyme primarily involved in SP hydrolysis, was also decreased in patients with duodenitis.. Based on these findings, we propose that decreased levels of VIP and CGRP and increased levels of SP contribute to pathological changes in gastric mucosa. Hence, new treatments targeting these molecules may have therapeutic and preventive effects.

Topics: Abdominal Pain; Adolescent; Calcitonin Gene-Related Peptide; Case-Control Studies; Child; Duodenitis; Endoscopy; Female; Gastric Mucosa; Gastritis; Humans; Hydrolysis; Immunohistochemistry; Male; Neprilysin; Neuropeptides; Substance P; Vasoactive Intestinal Peptide

The main goal of our research was to study the possible alterations of the chemical coding of the dorsal motor vagal nucleus (DMX) neurons projecting to the porcine stomach prepyloric region following prolonged acetylsalicylic acid supplementation. Fast Blue (FB) was injected into the studied area of the stomach. Since the seventh day following the FB injection, acetylsalicylic acid (ASA) was given orally to the experimental gilts. All animals were euthanized on the 28th day after FB injection. Medulla oblongata sections were then processed for double-labeling immunofluorescence for choline acetyltransferase (ChAT), pituitary adenylate cyclase-activating peptide (PACAP), vasoactive intestinal polypeptide (VIP), nitric oxide synthase (NOS), galanin (GAL), substance P (SP), leu enkephalin (LENK), and cocaine- and amphetamine-regulated transcript (CART). In the control DMX, only PACAP was observed in 30.08 ± 1.97 % of the FB-positive neurons, while VIP, NOS, GAL, SP, LENK, and CART were found exclusively in neuronal processes running between FB-labeled perikarya. In the ASA DMX, PACAP was revealed in 49.53 ± 5.73 % of traced vagal perikarya. Moreover, we found de novo expression of VIP in 40.32 ± 7.84 %, NOS in 25.02 ± 6.08 %, and GAL in 3.37 ± 0.85 % of the FB-labeled neurons. Our results suggest that neuronal PACAP, VIP, NOS, and GAL are mediators of neural response to aspirin-induced stomach inflammatory state.

Topics: Acetyltransferases; Animals; Aspirin; Enkephalin, Leucine; Galanin; Gastric Mucosa; Gastritis; Medulla Oblongata; Nerve Tissue Proteins; Neurons, Efferent; Nitric Oxide Synthase Type I; Pituitary Adenylate Cyclase-Activating Polypeptide; Stomach; Substance P; Swine; Vagus Nerve; Vasoactive Intestinal Peptide

The protective effect of capsaicin-sensitive sensory nerve (CSSN) activation was recently demonstrated in human gastric mucosa. We here examined changes in neuropeptides, specifically Substance P (SP), calcitonin-gene related peptide (CGRP) and vasoactive intestinal peptide (VIP) in patients with chronic gastritis or ulcer. Furthermore changes in neprilysin levels, which hydrolyse these neuropeptides, were determined. Gastric biopsies were obtained from both lesion- and normal-appearing mucosa of 57 patients. The presence of H. pylori infection was verified with rapid urease assay. Neuronal and non-neuronal levels of SP, VIP, CGRP and neprilysin activity were determined in freshly frozen biopsies. Immunohistochemical localization of neprilysin was performed in 30 paraffin embedded specimens. We here found that neuronal SP levels decreased significantly in normally appearing mucosa of patients with gastritis while levels of non-neuronal SP increased in diseased areas of gastritis and ulcer. The presence of H. pylori led to further decreases of SP levels. The content of VIP in both disease-involved and uninvolved mucosa, and expression of neprilysin, markedly decreased in patients with gastritis or ulcer. Since VIP, as well as SP fragments, formed following hydrolysis with neprilysin is recognized to have gastroprotective effects, decreased levels of VIP, SP and neprilysin may predispose to cellular damage.

Topics: Adult; Calcitonin Gene-Related Peptide; Duodenal Ulcer; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Neprilysin; Neurons; Peptic Ulcer; Substance P; Ulcer; Vasoactive Intestinal Peptide; Young Adult

Several neuropeptides were supposed to take place in the protection of gastric mucosa and play role in the development of gastritis.. To investigate morphological relationship between nerve fibres and immunocytes, to find out if these cells synthetize some neuropeptides and if there is there any co-existence with TNF-α and NFκ-B.. Immunohistochemical, confocal laser microscopic methods were used to investigate nerve fibres, immunocompetent cells in control and gastritis mucosa.. The number of neuropeptide-containing nerve fibres increased significantly. In control stomach the number of lymphocytes, plasma cells, and mast cells was low and showed no immunoreactivity for neuropeptide antibodies. However, in gastritis, some of the immunocompetent cells were immunoreactive for SP and for NPY. Some of the SP immunoreactive cells showed also positive reaction for TNF-α and NFκ-B. The distance between nerve fibres and immunocytes was 1 µm or less.. The increase of neuropeptides released from nerve fibres and immunocompetent cells can take part in neurogenic inflammation and generate chronic gastritis.

Topics: Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Lymphocytes; Mast Cells; Microscopy, Confocal; Nerve Fibers; Neuropeptide Y; NF-kappa B; Substance P; Tumor Necrosis Factor-alpha; Vasoactive Intestinal Peptide

To investigate the effect of Helicobacter pylori (H. pylori) infection on neuronal expressions in the stomach and spinal cord of mice so as to explain dyspepsia symptoms in H. pylori infected patients.. C57BL/6 female mice were studied at 2 weeks (acute infection group) and 12 weeks (chronic infection group) after H. pylori inoculation. Histological analyses for gastric inflammation and bacterial colonization were assessed by HE staining and Warthin-Starry staining. Fos, vasoactive intestinal polypeptide (VIP) and calcitonin gene-related peptide expressions (CGRP) were studied by immunohistochemistry.. H. pylori colonization was present mainly in pyloric region, but bacterial density was similar in both infected groups. The intensity of mucosal inflammation and activity was significantly higher in two infected groups than in those in the control group. The degree of mononuclear and polymorphonuclear cell infiltration in proventricular-glandular region and gastric corpus at 12 weeks after H. pylori inoculation was higher than that at 2 weeks after inoculation. The neuronal expressions of fos, VIP, and CGRP in the stomach and spinal cord were significantly more marked in the infected groups than in the control group, but there was no significant difference between two infected groups.. H. pylori infection induced different degrees of gastric mucosal inflammation in the murine model. Both early and chronic infection groups of mice showed enhanced neuronal expressions of fos, VIP and CGRP of stomach and spinal cord and these could form a basis for appearance of functional dyspeptic symptoms in patients with H. pylori infection.

Topics: Acute Disease; Animals; Calcitonin Gene-Related Peptide; Chronic Disease; Disease Models, Animal; Dyspepsia; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Immunohistochemistry; Mice; Neurons; Proto-Oncogene Proteins c-fos; Spinal Cord; Stomach; Vasoactive Intestinal Peptide

Neuromuscular changes producing dysmotility and hyperalgesia may underlie symptom generation in functional gastrointestinal disorders. We investigated whether chronic Helicobacter pylori-induced gastritis causes neuromuscular dysfunction.. In vitro muscle contractility and acetylcholine release were evaluated in mice before and after H. pylori eradication. H. pylori colonization and gastritis were graded histologically. Substance P (SP)-, vasoactive intestinal polypeptide (VIP)-, and calcitonin gene-related peptide (CGRP) immunoreactivity (IR) and macrophages were studied by immunohistochemistry.. In Balb/c mice, chronic H. pylori infection did not affect muscle function but augmented antral relaxation after nerve electric field stimulation. Infected mice had lower acetylcholine release by electric field stimulation and had higher density of SP-, CGRP-, and VIP-IR nerves in the stomach and of SP- and CGRP-IR in the spinal cord. Cholinergic nerve dysfunction worsened progressively and was associated with increasing macrophage and mononuclear but not polymorphonuclear infiltrate or bacterial colonization. SCID mice had unchanged acetylcholine release despite high H. pylori colonization and macrophage infiltration. Eradication of H. pylori normalized functional and morphologic abnormalities except for increased density of gastric SP- and CGRP-IR nerves.. H. pylori infection induces functional and morphologic changes in the gastric neural circuitry that are progressive and lymphocyte dependent, and some persist after H. pylori eradication. The data have direct implications regarding the role of H. pylori infection in functional dyspepsia.

Topics: Acetylcholine; Animals; Calcitonin Gene-Related Peptide; Disease Models, Animal; Enteric Nervous System; Female; Gastritis; Helicobacter Infections; Helicobacter pylori; Immunohistochemistry; Macrophages; Mice; Mice, Inbred BALB C; Mice, SCID; Muscle Contraction; Specific Pathogen-Free Organisms; Spinal Cord; Stomach; Substance P; Vasoactive Intestinal Peptide

The synthetic peptides AC-Glu-Phe-Phe (NO2)-Arg-amide (peptide VP) and AC-Ile-Glu-Phe-Phe (NO2)-Arg-amide (peptide VIP) are more readily hydrolyzed by human pepsin in gastric juice of patients of gastritis than those of duodenal ulcer and normal subjects. The kinetic parameters suggest that S3 subsite of the enzyme plays a role in the elevation of enzyme activity in gastric disease.

Topics: Amino Acid Sequence; Binding Sites; Duodenal Ulcer; Gastric Juice; Gastritis; Humans; Kinetics; Molecular Sequence Data; Oligopeptides; Pepsin A; Reference Values; Substrate Specificity; Vasoactive Intestinal Peptide