Gastrin and somatostatin in Helicobacter pylori infected antral mucosa.

Ødum, Lars; Petersen, Hans Draminsky; Andersen, Ida Brandt; Hansen, Birgit Fischer; Rehfeld, Jens F.

doi:10.1136/gut.35.5.615

Cited by 62 publications

(32 citation statements)

References 27 publications

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“…Our observation that treatment with Hp WE significantly attenuated gastric luminal release of somatostatin is in keeping with the previous observation that luminal somatostatin levels as well as mucosal expression of somatostatin mRNA were significantly decreased in Hp -infected human gastric mucosa [41]. It has been suggested that the facilitated gastrin release in Hp - infected patients may be the result of a reduced or blocked release of antral somatostatin, but the underlying mechanism has not been explained [42]. Hypergastrinemia, observed in Hp -infected mucosa, was attributed to either inflammatory cytokines [43]and/or alkalinization of the antral part of the stomach due to the local rise in antral pH by prolonged elevation of ammonia in the gastric juice caused by the urease activity of Hp [44, 45].…”

Section: Discussionsupporting

confidence: 78%

Water Extracts of Helicobacter pylori Delay Healing of Chronic Gastric Ulcers in Rats: Role of Cytokines and Gastrin-Somatostatin Link

Brzozowski

Konturek

et al. 1999

Digestion

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Background: Helicobacter pylori (Hp) is considered as a major risk factor of peptic ulcer, but the pathogenic mechanism of its action has not been fully explained. Aims: This study was designed: (1) to compare the ulcer healing effects of water extract (WE) obtained from type-I cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) expressing Hp and from type-II CagA- and VacA-negative Hp strain with those of vehicle (saline), and (2) to determine the alterations in gastric secretion, gastric blood flow (GBF) and expression of Hp-related cytokines during the ulcer healing in rats treated with toxigenic (type-I) and non-toxigenic (type-II) Hp-derived WE. Methods: Gastric ulcers were produced by serosal application of acetic acid in rats with or without gastric fistula treated with vehicle (saline) or WE originating from type-I or type-II Hp administered intragastrically on days 1, 3, 5 and 7 upon ulcer induction. On days 3, 9 and 15, animals were lightly anesthetized with ether, the abdomen was opened and the GBF was measured by the H₂-gas clearance technique in the ulcer area and non-ulcerated mucosa. Venous blood was withdrawn for the measurement of plasma cytokine (IL-1β and TNFα) levels and plasma and gastric contents were also collected for gastrin and somatostatin determination by specific radioimmunoassay. Results: Gastric ulcers healed gradually in vehicle-treated controls and the ulcer area on days 3, 9 and 15 was reduced by 12, 43 and 92%, respectively. In rats treated with WE of type-I Hp, ulcer healing was significantly delayed, and gastritis and infiltration of ulcerated gastric mucosa with inflammatory cells were observed histologically. The prolongation of ulcer healing by WE of both Hp strains was accompanied by a marked fall in the GBF at the ulcer margin and transient hyposecretion especially in rats given WE of type-I Hp strain. On day 15 of ulcer healing, the plasma concentration of IL-1β and TNFα was negligible in vehicle control rats, but it was significantly elevated particularly in rats treated with WE of type-I Hp. RT-PCR analysis revealed that mucosal expression of IL-1β and TNFα mRNA was significantly upregulated in the gastric mucosa of rats treated with either toxigenic or non-toxigenic Hp WE. The plasma gastrin level was significantly higher and the luminal concentration of somatostatin was significantly lower in rats treated with Hp-WE than in vehicle-treated controls and these alterations were more pronounced in rats treated with WE type-I than type-II Hp. Conclusions: WE of toxigenic Hp strain delays ulcer healing due to the reduction in the gastric microcirculation at the ulcer margin, the overexpression of inflammatory cytokines and the impairment of the gastrin-somatostatin link.

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Section: Discussionsupporting

confidence: 78%

Water Extracts of Helicobacter pylori Delay Healing of Chronic Gastric Ulcers in Rats: Role of Cytokines and Gastrin-Somatostatin Link

Brzozowski

Konturek

et al. 1999

Digestion

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“…Interestingly, the microflora also regulates gastrointestinal endocrine cells and the synthesis and/or release of neuroendocrine peptides and the amine serotonin which, in turn, may affect cell proliferation in the gastrointestinal epithelium [6]. Likewise, H. pylori infection is associated with a reduced volume density of somatostatin-immunoreactive cells in the antral mucosa [37] and with low tissue concentrations of this peptide [38]. Somatostatin is a potent inhibitor of cell proliferation, which implies that a reduced inhibitory drive on the proliferative compartments secondary to reduced availability of the peptide may have contributed to the increase in cell proliferation observed in the gastric mucosa of patients infected with H. pylori [24].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Stimulates DNA Synthesis in a Small Intestinal Cell Line in vitro

Brännström

Zachrisson²,

Hultén³

et al. 1998

Digestion

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Background: Helicobacter pylori, which causes gastritis and peptic ulcer, seems to be an important factor in the pathogenesis of gastric cancer and MALT lymphoma. Thus our aim was to examine whether H. pylori influences DNA synthesis in epithelial cells in vitro. Methods: Sonicated and water extracts of H. pylori (cytotoxic strains NCTC 11637, 88-23 and A5, and a noncytotoxic isogenic mutant of A5, A5 vac A) were diluted to a final concentration of 1/1,000, 1/100, 1/50 and 1/10. Water extracts of Escherichia coli were used as reference. IEC-6 cells were incubated during 24 h with fragments of H. pylori or extracts of the concentrations described above. The cells were labeled with ³H-methylthymidine for 4 h and processed for autoradiography. DNA synthesis was evaluated by the labeling index (LI). Results: The LI% of controls was 15.6 ± 5.1%. All the water extracts and sonicated strains of H. pylori increased the LI% in a dose-dependent manner (p < 0.001). The highest concentrations of the sonicated strains tended to reduce the LI%, although these values were still higher than those of the control group. The water extracts of E. coli increased the LI% in a dose-dependent manner (p < 0.0001). Conclusion: H. pylori stimulates DNA synthesis in epithelial cells in vitro, but no association was found with the presence of cytotoxin production. Our results suggest that hitherto unknown components of H. pylori may contribute to the increase in cell proliferation observed in gastritis and to the development of MALT lymphoma and gastric cancer.

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“…A subsequent explanation for hypergastrinemia has been proposed with the demonstration of the impaired synthesis and release of somatostatin by H. pylori . Since somatostatin in the stomach acts to suppress gastrin release, its reduction results in the loss of the paracrine control of gastrin release and thus to hypergastrinemia [13,14]. …”

Section: Acid Secretion In Peptic Ulcer Diseasementioning

confidence: 99%

The Intriguing Relationship of Helicobacter pylori Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

Malfertheiner

2011

Dig Dis

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Helicobacter pylori infection induces chronic inflammation of the gastric mucosa and thus profoundly affects gastric physiology. In the acute phase of infection, gastric acid secretion is transiently impaired. The morphological damage of the gastric mucosa, changes in gastric hormone release, and disruption of neural pathways all contribute to influence gastric acid secretion in a distinct manner. Changes in gastric acid secretion, whether impaired or increased, are intimately related with the topographic phenotypes of gastritis and the presence of atrophy or absence of corpus atrophy. The interplay of gastritis phenotype and acid secretion are key determinants in disease outcomes. Corpus-predominant gastritis and corpus atrophy are accompanied by hypochlorhydria and carry the highest risk for gastric cancer, whereas antrum-predominant gastritis with little involvement of the corpus-fundic mucosa is associated with hyperchlorhydria and predisposes to duodenal ulcer disease.

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Gastrin and somatostatin in Helicobacter pylori infected antral mucosa.

Cited by 62 publications

References 27 publications

Water Extracts of <i>Helicobacter pylori</i> Delay Healing of Chronic Gastric Ulcers in Rats: Role of Cytokines and Gastrin-Somatostatin Link

Water Extracts of <i>Helicobacter pylori</i> Delay Healing of Chronic Gastric Ulcers in Rats: Role of Cytokines and Gastrin-Somatostatin Link

Helicobacter pylori Stimulates DNA Synthesis in a Small Intestinal Cell Line in vitro

The Intriguing Relationship of <i>Helicobacter pylori</i> Infection and Acid Secretion in Peptic Ulcer Disease and Gastric Cancer

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