Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Campylobacter pylori (C.p.) infection is often found in patients with antral gastritis and peptic ulcer disease. Pathophysiological links are still unclear, and we therefore tested the hypothesis whether C.p. affects the gastrointestinal peptides and thus influences gastric acid secretion and protective factors. 94 patients were examined by upper GI endoscopy and blood analyzed for gastrin, somatostatin, pancreatic polypeptide and neurotensin. Biopsies of antral mucosa were investigated for C.p. in urease testing, culture and microscopy. C.p. was found in 42 patients (45%). In microscopy all of these patients had chronic gastritis (100%). A significant increase in gastrin uninfluenced by C.p. was found in patients with antral gastritis (normal: 6.4 +/- 0.7, [n = 27]; gastritis without C.p.: 18.4 +/- 5.9 [p less than 0.02], [n = 7]; gastritis with C.p.: 10.7 +/- 2.2, [n = 22]). Somatostatin, pancreatic polypeptide and neurotensin showed no difference.
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PMID:[Campylobacter pylori colonization of the antrum: effect of gastrin, somatostatin, pancreatic polypeptide and neurotensin]. 256 33

Helicobacter pylori is a microaerophilic bacterium initially found in the gastric antrum of patients with peptic ulcer disease. As a result, H. pylori is now believed to have a pathophysiologic role in gastritis as well as in peptic ulcer disease. Several recent studies showed that it may be associated with duodenal ulcer relapse and that eradication therapy using antibiotics may significantly decrease the ulcer recurrence rate in duodenal ulcer patients. Moreover, epidemiological studies suggest that it may increase the relative risk of carcinoma in the stomach and preliminary studies seem to indicate that some low-grade lymphoma in the stomach may regress after H. pylori eradication. Although the mechanisms by which H. pylori induces mucosal injury and/or neoplasm is not clearly understood, several modifications in gastric functions have been reported. The most specific way of detecting H. pylori in tissue is a combination of culture and histologic staining of mucosal biopsy specimens obtained by endoscopy. Rapid urease test, cytology and PCR procedures performed on biopsies may give rapid, sensitive and specific results. Breath test using 13C- or 14C-radiolabelled urea and serology tests are of particular importance when H. pylori diagnosis is needed via no invasive procedures. Helicobacter pylori is supposed to interact with G and D cells. Gastrin and somatostatin are synthetized and released from antral G and gastric D cells respectively. The gastric D cells are in close contact with either G and parietal cells. Gastrin stimulates gastric acid secretion and epithelial gastric cell proliferation (parietal and EC-L cells) while somatostatin inhibits these effects. Chronic gastritis is associated with fundic duodenal ulcer disease. In this situation, basal gastrin and meal- or bombesin-stimulated gastrin in the serum (especially gastrin G17) have been found to be higher in H. pylori positive than in negative patients. Moreover, gastrin decreases up to normal levels after eradication of H. pylori. The long term effect of a such hypergastrinemia is not so far established. The mechanism underlaying hormonal modification is poorly understood. Since no G/D cell ratio modification could be found after H. pylori eradication while the amount of somatostatin increases, one would suggest functional alteration of either G or D cells in the H. pylori-related chronic gastritis. The role of inflammatory mediators on the gastrin release and the processing of progastrin induced by the bacterium need further investigations.
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PMID:[Helicobacter pylori, a rediscovered bacterium. Implication in gastroduodenal diseases]. 789 50

Antral gastrin cell hyperfunction (AGCH) is a rare syndrome characterized by persistent hypergastrinemia and important peptic symptoms in the absence of a gastrin-producing tumor. The pathogenesis of AGCH is still unknown and debated. Helicobacter pylori (Hp) infection has been reported as a possible cause of sustained hypergastrinemia. To assess the relevance of Hp infection in pediatric AGCH patients, Hp status, G cell function, acid secretion, and antral G and D cell populations were investigated in six children presenting with gastrointestinal bleeding of unknown origin, sideropenic anemia, and variable abdominal symptoms. All patients had moderate high basal gastrinemia with abnormally increased peak values after meals and elevated values of basal acid output (BAO), maximal acid output (MAO), and pentagastrin-stimulated acid output (PAO). Circulating pepsinogen I was also significantly increased. Three children had Hp infection, as assessed by enzyme-linked immunosorbent assay, urease test, and histology. Endoscopy showed duodenal erosions in three children, with ulcer in two Hp-positive cases. At histology, moderate gastritis was observed only in the three Hp-positive cases. In all patients, quantitative assessment of antral gastrin and somatostatin cells gave significantly elevated G cell counts; D cells were at the lower reference limit and the G/D cell ratio was significantly elevated. These data indicated a diagnosis of AGCH, possibly due to the elevated G/D cell ratio, and suggest HP infection as an overlapping factor complicating the clinical picture in some cases.
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PMID:Helicobacter pylori infection in children with antral gastrin cell hyperfunction. 791 67

The authors review recent progresses made in the understanding of the disturbed gastrin homeostasis in Helicobacter pylori infection and in pernicious anaemia. Regulation of gastrin release in a complex mechanism involving inhibition by a low gastric pH and several peptides including somatostatin, and stimulation by different factors, mainly alimentary peptides and amino-acids. The hypergastrinaemia observed in patients with Helicobacter pylori infection occurs despite a normal intraluminal pH. This may be through alkalinisation of the gastric mucus layer due to the production of ammonia by the bacterial urease or through local release of inflammatory mediators. In pernicious anaemia a factor present in the antacid gastric juice could explain the important hypergastrinaemia observed. The gastrin releasing activity of the gastric juice itself was demonstrated by a decrease of the patients' plasma gastrin concentration during a neutral gastric lavage and by a rise of the gastrin levels in rats whose stomachs were perfused with gastric juice from pernicious anaemia patients. A better understanding of the relation between gastric pH and gastrin release is important not only for these pathological states but also for treatments which suppress acid secretion.
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PMID:[Mechanisms in hypergastrinemia in autoimmune atrophic gastritis and Helicobacter pylori infection]. 826 64

Research is asking how H. pylori causes diseases, and also why the same bacteria produces different conditions in different persons. The process involves bacterial factors and the host's response. Some bacterial factors such as urease are produced by all strains of H. pylori. This enzyme may damage the gastric epithelium by practically releasing ammonia. Other bacterial factors such as vacuolating toxin are only produced by some strains, and these strains are more likely to cause ulcers or cancer. The host's response has been studied by physiologists, immunologists, and histologists, but the separation of systems is artificial. For example, physiologists find that H. pylori stops gastric D-cells from expressing somatostatin normally, which impairs reflex inhibition of acid secretion, but the D-cell malfunction is probably due to inflammatory factors. In H. pylori gastritis, the gastric epithelial cells behave like immunocytes and express class II molecules and cytokines such as interleukin-8. The patient's histological response to H. pylori is quite closely related to the disease outcome. Patients who respond by developing gastric atrophy are more likely to get gastric ulcers or stomach cancer, but patients whose gastric corpus remains healthy tend to secrete more acid and develop duodenal ulcers, particularly if they have gastric metaplasia in their duodenum. Studies of disease mechanisms provide a valuable insight into the development of these common diseases, and may enable us to identify at-risk groups who particularly merit eradication therapy.
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PMID:Pathogenic mechanisms. 856 49

Helicobacter pylori is highly adapted to its unusual ecological niche in the human stomach. Urease activity permits H. pylori survival at a pH of <4 in vitro and is required for the organism to colonize in animal models. However, urease does not play an important role in the survival of the organism in a pH range between 4 and 7. Other mechanisms of pH homeostasis remain poorly understood, but preliminary studies indicate that novel proteins are produced when H.pylori cells are shifted from pH 7 to 3, and the gene encoding a P-type adenosine triphosphatase that may catalyze NH4+/H+ exchange across the cytoplasmic membrane has been cloned. Mechanisms of pH homeostasis in other enteric bacteria are reviewed and provide insight into additional pathways that may be used by H. pylori. An important adaptation of H. pylori to the gastric environment may be its ability to alter gastric acid secretion. Acute infection is associated with transient hypochlorhydria, whereas chronic infection is associated with hypergastrinemia and decreased somatostatin levels. Thus, the survival of H. pylori in the gastric environment may be attributed to both the development of specialized intrinsic defenses and the organism's ability to induce physiological alterations in the host environment.
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PMID:Helicobacter pylori and gastric acid: biological and therapeutic implications. 878 Jun

The aim of this study was to investigate the consequence of Helicobacter pylori eradication on gastric mucosa and antral G and D-cells. Forty children, aged 5-17 years with Helicobacter pylori infection were assessed. Helicobacter pylori was detected by a urease test and identified by serological and microbiological methods. Twenty children were again assessed after the therapy (the combination of colloid bismuth subcitrate, amoxycillin and metronidazole). Gastroscopic examination was performed and at least six bioptic specimens were taken from the antrum, body and fundus. Tissue samples, processed with the paraffin method and stained with hematoxyllin and eosin, were assessed. Monoclonal antiserum Gastrin PAP kit 516 and somatostatin PAP kit 512 (DAKO) in the peroxidase-antiperoxidase technique (PAP) have been used to detect G and D-cells. Helicobacter pylori in the gastric mucosa was demonstrated with the Giemsa method. The results show the coincidence of Helicobacter pylori infection and the count of antral G and D-cells and active chronic gastritis in children. After the treatment Helicobacter pylori was eradicated in 70% of children. In 34% of these cases the eradication was followed by a diminution of activity of gastric antral mucosa inflammation and in 20% of these children the resolution of the inflammatory infiltration in the gastric mucosa was seen. A decrease of the antral G and D-cells count and also a diminution of G/D index in these cases were observed.
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PMID:Morphological and immunohistochemical examinations of the dynamic changes of gastric mucosa associated with the treatment of helicobacter pylori infection in children. 877 26

Infection with Helicobacter pylori (H. pylori) is now recognized as a major factor in the pathogenesis of gastric disease, and the successful therapy regimens require a combination of H2 blockers with gastroprotective and antimicrobial agents. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene) amino]-4-thiazolyl] methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamide, CAS 100981-43-9, FI-3542) is the only drug combining acid-suppressant activity with remarkable gastroprotective and anti-H. pylori properties. The drug not only displays a potent anti-H. pylori activity alone, but also exerts a strong potentiating effect on the efficacy of antimicrobial agents commonly used for H. pylori eradication, and the successful ulcer therapy with ebrotidine induces a significant (4-fold) increase in the H. pylori aggregation titer of gastric mucin. Moreover, the drug exhibits a strong inhibitory effect on H. pylori urease activity, the extent of which exceeds that of ranitidine, omeprazole and lansoprazole. Ebrotidine has also been demonstrated to exert a potent inhibitory action on the enzymatic activities directed towards mucus perimeter of gastric mucosal defense, causing a marked inhibition of H. pylori protease, lipase and phospholipase A2 activities. Another important property of ebrotidine is its ability to efficiently counteract the disruptive effects of H. pylori lipopolysaccharide on the integrity of gastric epithelium. This includes countering the interference by the lipopolysaccharide in mucosal integrin receptor interaction with proteins of extracellular matrix and the reversal of H. pylori disruptive effect on the binding of mucin to its gastric epithelial receptor. Furthermore, most recent data indicate that ebrotidine has the ability to reverse the impairment caused by H. pylori in feedback inhibition of gastrin release by somatostatin. This activity of ebrotidine apparently stems from the drug's ability to counter the untoward effect of H. pylori on the binding of somatostatin to its specific receptor on the gastric mucosal G-cells. The unique combination of acid suppressant, gastroprotective and anti-H. pylori activities makes ebrotidine a drug of choice in the treatment of gastric disease caused by H. pylori.
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PMID:Anti-Helicobacter pylori activities of ebrotidine. A review of biochemical and animal experimental studies and data. 920 47

Helicobacter pylori (Hp) is a major risk factor of peptic ulcer but studies on the relation between Hp infection and gastric pathology are limited due to lack of convenient models resembling Hp infection in humans. We studied the effects of inoculation of conventional BALB/c mice with toxigenic type I Hp (cagA+ and vacA+) and non-toxigenic type II Hp (cagA- and vacA-) vs administration of vehicle on gastric secretion and healing of gastric ulcers. The gastric secretion studies were performed on mice with chronic gastric fistula before and after inoculation with toxigenic or non-toxigenic Hp strain or administration of vehicle (saline). Gastric ulcers were produced in mice inoculated with toxigenic and non-toxigenic Hp strain or vehicle and then sacrificed at day 0 and after 2, 4, 7, 14 and 28 days. Ulcer area and gastric blood flow (GBF), plasma gastrin and gastric luminal somatostatin were determined. Gastric mucosal biopsy specimens were also taken for the assessment of the presence of viable Hp using rapid urease test, the Hp-culture and the reverse transcriptase--polymerase chain reaction (RT-PCR) analysis of the signal for Hp CagA. Gastric acid output was reduced by over 50% immediately after Hp inoculation and this effect persisted during all time intervals tested, being significantly more pronounced in type I Hp-infected stomach. The area (7 mm2) of ulcers in control mice decreased gradually and then continued to decline during 14 days to disappear almost completely after 28 days. In contrast, the ulcers were present till day 28 in all mice infected with type I or type II Hp strain being significantly larger especially with type I Hp-infection. The GBF in control mice showed gradual rise with decreasing ulcer size being significantly higher at the ulcer margin than the ulcer crater and reached after 14 and 28 days the value not significantly different from that in vehicle-administered mice. In contrast, the GBF in type I Hp-infected mice but to a lesser extent, in type II Hp infected mice was significantly lower than in the vehicle controls, both at the ulcer margin and the crater of ulcers at all tested days. Hp-infection was accompanied by significant increment in plasma gastrin and the fall in gastric somatostatin contents observed at all test days, particularly in mice infected with type I Hp strain. Edema of surface epithelium appeared after 7 days and wak but significant mucosal inflammatory infiltration occurred after 14 days to further increase after 28 days, especially in type I Hp and less in type II Hp infected mice. We conclude that conventional mice with gastric ulcers can be successfully infected by both toxigenic and non-toxigenic Hp strains and this infection markedly reduces gastric acid secretion and delays healing of ulcers probably due to the fall in mucosal microcirculation in ulcer area, mucosal inflammation and impairment in gastric-somatostatin link.
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PMID:Gastric secretion and ulcer healing in mouse stomach infected with cytotoxin expressing strain of Helicobacter pylori. 978 92

The protection of Helicobacter pylori from the gastric acid exerted by urease is based on an increase of the bacterial periplasmic pH and membrane potential. Ammonia generated from urea induces apoptosis of gastric cells in vitro, and inhibits gastric somatostatin release in animals, which could have consequences on the physiology of digestion in general. The type s1/m1 structure of the vacA gene is associated with the production of high levels of cytotoxin. Strains with m2 region type, formerly considered devoid of toxic activity, are fully toxic when assayed with cell lines other than HeLa cells, which possibly lack receptors for m2 VacA type. The enhanced gastric mucosa damage associated with infection by cytotoxic organisms could be explained by the varying of effects exerted by VacA on target cells: extracellular secretion of acidic hydrolases, cytoskeletal alterations, actin rearrangement, reduction of epidermal growth factor binding to its receptor, inhibition of the stimulation of CD4+ T cells proliferation induced by the antigen presenting cells. Organisms that possess the pathogenicity island cag (cag+) induce an increased inflammation and transduction of signals to the host cells; however, they reduce the apoptosis of colonised cells. The results of an investigation on the possible influence of a variable cagA status on the extension of apoptosis have indicated that this kind of programmed death is disengaged from the possession of cagA by Helicobacter pylori organisms colonising the same gastric areas. It is likely that the whole pathogenic potential of cag+ organisms is far from being completely explored, as suggested by the recent finding that the expression of a bacterial adhesin (called BabA) involved in binding to the blood group antigen Lewis b is associated with the presence of cag.
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PMID:New acquisitions in Helicobacter pylori characteristics. 1007 48


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