Antigen-Induced Gastrin Release: An Immunologic Mechanism of Gastric Antral Mucosa

Krämling, H.-J.; Enders, G.; Teichmann, R.; Demmel, T.; Merkle, R.; Brendel, W.

doi:10.1007/978-1-4684-5344-7_49

Cited by 20 publications

(5 citation statements)

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“…There are several reports regarding the role of cytokines, which are released by the inflammatory cells activated by H. pylori , in the regulation of antral G-cell function. These reports have suggested that interleukins, TNF- α or interferons stimulate gastrin secretion via receptors potentially residing on antral G-cells 36 – 38 ) .…”

Section: Discussionmentioning

confidence: 99%

Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

Park

Lee

Kim

et al. 1999

Korean J Intern Med

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ObjectivesHelicobacter pylori infection induces selective reduction of the number of antral D-cells and results in abnormal regulation of serum gastrin secretion. The purpose of this study was to investigate the relationship between H. pylori infection and the numbers of G-cells and D-cells.MethodsThe numbers of antral G-cells and D-cells, the ratio of G-cells to D-cells and fasting serum gastrin concentrations were compared between 37 patients with (29 with duodenal ulcers and 8 with gastric ulcers) and 33 without H. pylori infection (22 with duodenal ulcers and 11 with gastric ulcers). Serum gastrin concentrations were measured using the radioimmunoassay technique. Antral mucosal biopsy specimens were examined using immunohistochemical staining with antibodies specific for gastrin and somatostatin and the numbers of G-cells and D-cells per gastric gland were counted.ResultsFasting serum gastrin concentrations were significantly higher in patients with H. pylori infection compared to patients without infection (80.3±23.5 vs 47.6±14.1 pg/ml, p<0.001). The number of G-cells per gastric gland was similar in infected and uninfected patients (7.1±3.1 vs 7.3±3.9, respectively, p>0.5). The number of D-cells was significantly lower in patients with H. pylori infection than in uninfected patients in both duodenal and gastric ulcer patients (1.3±0.4 vs 2.5±1.6, respectively, p<0.001). The ratio of G-cells to D-cells was also significantly higher in infected patients compared with uninfected patients for both gastric and duodenal ulcers (5.7±2.7 vs 3.5±1.9, respectively, p<0.001).ConclusionsThese results strongly suggest that Helicobacter pylori infection induces reduction of the number of antral D-cells. The resulting relative hypofunction of the inhibitory action of D-cells against G-cells may be responsible for increased serum gastrin secretion.

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Section: Discussionmentioning

confidence: 99%

Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

Park

Lee

Kim

et al. 1999

Korean J Intern Med

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“…Statistical analysis was used by the Mann-Whitney U Test. The percent of Bad protein in case group showed significant increase to control group (p = 0.0001) whereas a further fall in the levels of LNA was observed [36].…”

Section: Discussionmentioning

confidence: 78%

Dietary PUFA Increase Apoptosis in Stomach of Patients with Dyspeptic Symptoms and Infected with H. pylori

Sharifi

Nouri

Eidi

et al. 2017

Lipids

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Drug-resistant strains of Helicobacter pylori and poor treatment response are the main reasons for the failure in eradicating it in patients. Polyunsaturated fatty acids (PUFA) have an inhibitory effect on bacterial growth. The aim of this study was to investigate the effect of PUFA in combination with standard triple therapy on apoptosis in H. pylori infected subjects with dyspeptic symptoms. This study was a double-blind clinical trial in which 34 H. pylori infected subjects with dyspeptic symptoms were randomly divided into two groups of 17 patients. The control group received standard triple therapy (amoxicillin, clarithromycin and omeprazole) and the experimental group received the standard therapy and PUFA for two weeks. Gene expression levels of caspase-3, BCL-2 and Bad proteins were studied with real-time PCR, while protein levels were quantified in frozen sections and using immunohistochemistry. Compared with the control group, a significant increase (p < 0.01) was observed in the expression of caspase-3 and Bad genes and a significant reduction (p < 0.05) in the expression of Bcl-2 gene. The protein level of active caspase-3 and Bad protein was significantly increased and the level of Bcl-2 protein was significantly decreased (p < 0.05). The results of this study show that oral administration of PUFA in combination with the standard triple therapy increased apoptosis in H. pylori-infected patients with dyspeptic symptoms. This increase in apoptosis may partly reduce drug resistance in these patients. Our results suggest inclusion of a dietary PUFA containing fatty acid supplement may improve treatment of patients that are refractory to the standard triple therapy.

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“…Further, gastrin release could also be demonstrated in vitro after antigenic challenge of antral cell preparations [5,6], thus demonstrating local mechanisms of antigen specific reactions. The mediators responsible for this immunological effect are still unclear.…”

Section: Discussionmentioning

confidence: 89%

Mediators of antigen-induced gastrin release: role of antigen-antibody complexes and the complement system

et al. 1997

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That orally administered antigen was shown to induce gastrin release in immunized animals was a new aspect of gastrointestinal physiology. The mediators responsible for this immunological effect are still unclear. In an attempt to discover more about the mechanisms regarding antigen-induced gastrin release, we developed an in vitro system where fragments of rat antral mucosa were challenged. This makes it possible to determine the role of antigen-antibody complexes and the complement system in the mechanism of antigen-induced gastrin release. Wistar rats were immunized in vivo with NIP-OVA and mucosal fragments were challenge, in vitro with NIP-HGG. Gastrin was determined after a preincubation and a challenged incubation period without supernatants. After antigenic challenge, supernatants were used for in vitro challenge in order to rule out the presence of a soluble mediator and activation of complement. In a second group of experiments Wistar rats were used to study in vitro the release of specific antibodies after antigenic challenge. With this experimental design we were able to show increased gastrin secretion after antigenic challenge in vitro in the presence of intact tissue. It is shown that the increased gastrin release is most probably mediated by activation of the complement system in the presence of antigen-antibody complexes. These are built up by specific anti-NIP antibodies and NIP-HGG used for the challenge. The complement system might be the final pathway of the observed increased gastrin release.

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Antigen-Induced Gastrin Release: An Immunologic Mechanism of Gastric Antral Mucosa

Cited by 20 publications

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Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

Effect of Helicobacter pylori infection on antral gastrin and somatostatin cells and on serum gastrin concentrations

Dietary PUFA Increase Apoptosis in Stomach of Patients with Dyspeptic Symptoms and Infected with H. pylori

Mediators of antigen-induced gastrin release: role of antigen-antibody complexes and the complement system

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