Stimulation of pepsinogen release from chief cells byHelicobacter pylori: evidence for a role of calcium and calmodulin

Beil, Winfried; Wagner, Siegfried; Piller, M; Heim, Hans-Karl; Sewing, Karl–Friedrich

doi:10.1006/mpat.1998.0225

Cited by 3 publications

(6 citation statements)

References 21 publications

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“…In agreement with our results, Beil and colleagues 20 showed that both dbc AMP and 12-O-tetradecanoylphorbol-13-acetate, a phorbol ester activator of protein kinase C, increased the stimulus of H pylori on pig chief cell monolayers. Moreover, secretion was inhibited with both lanthanum and W-7.…”

Section: Discussionsupporting

confidence: 93%

“…However, we did not find differences in pepsinogen secretion using either cagA (+) H pylori or cagA (−) H pylori strains, suggesting that other factors must be involved. A recent study carried out in vitro on pig chief cell monolayer cultures 20 showed that VacA and CagA proteins do not affect H pylori induced pepsinogen secretion. However, Chan and colleagues 21 showed that pretreatment of human gastric adenocarcinoma cells with purified vacuolating toxin induced a concentration dependent release of pepsinogen.…”

Section: Discussionmentioning

confidence: 97%

“…This may be because the rise in dbc AMP stimulated peptic secretion depends mainly on adenylyl cyclase activation but also on calcium dependent intracellular signals. 20 Beil and colleagues 20 showed that dbc AMP stimulated secretion decreased with H-8, a protein kinase A inhibitor, but also with lanthanum and W-7, a calmodulin antagonist, suggesting that pepsinogen secretion induced by dbc AMP was partially regulated by the calcium-calmodulin system.…”

Section: Discussionmentioning

confidence: 99%

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Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

Lorente

Doiz²,

Serrano³

et al. 2002

Gut

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Background: Different acid and peptic related gastroduodenal diseases are associated with both increased gastric secretion and Helicobacter pylori infection. Patients with H pylori associated gastritis or duodenal ulcer have increased serum pepsinogen levels which decrease after eradication. The mechanisms of H pylori induced gastric mucosal damage are not completely understood. Aim: To determine the effects of H pylori on pepsinogen secretion from isolated human peptic cells. Methods: Dispersed human peptic cells were prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and density gradient centrifugation. H pylori was obtained from gastric biopsies (antrum and body), and cultured in non-selective and selective media. Isolates of H pylori were used at different concentrations (1-20×10 6 colony forming units (cfu)).Results: H pylori (10

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

Lorente

Doiz²,

Serrano³

et al. 2002

Gut

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“…It is interesting that calcium channel blockers are also associated with gastroesophageal reflux disease, probably due to its relaxation effect on lower esophageal sphincter [15]. HP infection can induce pepsinogen release from chief cells (which may induce and aggravate peptic ulcer disease) via mechanisms involving calcium and calmodulin [16]. However, L-type calcium channel is not responsible for the pepsinogen release induced by HP [16].…”

Section: Discussionmentioning

confidence: 99%

Diabetes, insulin use and Helicobacter pylori eradication: a retrospective cohort study

Tseng

2012

BMC Gastroenterol

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BackgroundDiabetic patients may have a higher risk of gastric cancer. However, whether they have a higher incidence of Helicobacter pylori (HP) eradication is not known. Furthermore, whether insulin use in patients with type 2 diabetes may be associated with a higher incidence of HP eradication has not been investigated.MethodsThis is a retrospective cohort study. The reimbursement databases from 1996 to 2005 of 1 million insurants of the National Health Insurance in Taiwan were retrieved. After excluding those aged <25 years, cases of gastric cancer, cases receiving HP eradication before 2005, patients with type 1 diabetes mellitus and those with unknown living region, the reimbursement data of a total of 601,441 insurants were analyzed. Diabetes status and insulin use in patients with type 2 diabetes before 2005 were the main exposures of interest and the first event of HP eradication in 2005 was the main outcome evaluated. HP eradication was defined as a combination use of proton pump inhibitor or H2 receptor blockers, plus clarithromycin or metronidazole, plus amoxicillin or tetracycline, with or without bismuth, in the same prescription for 7-14 days. The association between type 2 diabetes/insulin use and HP eradication was evaluated by logistic regression, considering the confounding effect of diabetes duration, comorbidities, medications and panendoscopic examination.ResultsIn 2005, there were 10,051 incident cases receiving HP eradication. HP eradication was significantly increased with age, male sex, diabetes status, insulin use, use of calcium channel blocker, panendoscopic examination, hypertension, dyslipidemia, chronic obstructive pulmonary disease, stroke, nephropathy, ischemic heart disease and peripheral arterial disease. Significant differences were also seen for occupation and living region. Medications including statin, fibrate, angiotensin-converting enzyme inhibitor/angiotensin receptor blocker and oral anti-diabetic agents were not associated with HP eradication. The adjusted odds ratios for diabetes, insulin use and use of calcium channel blocker was 1.133 (1.074, 1.195), 1.414 (1.228, 1.629) and 1.147 (1.074, 1.225), respectively.ConclusionsType 2 diabetes and insulin use in the diabetic patients are significantly associated with a higher incidence of HP eradication. Additionally, use of calcium channel blocker also shows a significant association with HP eradication.

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“…/ calmodulin-dependent protein kinase (7,21,22). Thus, we examined whether CaMK II activation by H. pylori is involved in the signaling pathway of IL-8 production.…”

Section: +mentioning

confidence: 99%

Protein Kinase C Activation by Helicobacter pylori in Human Gastric Epithelial Cells Limits Interleukin-8 Production Through Suppression of Extracellular Signal-Regulated Kinase

et al. 2004

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Abstract.Helicobacter pylori (H. pylori) infection of gastric epithelial cells has been shown to induce interleukin (IL)-8 production, but the signal transduction mechanism leading to IL-8 production has not been clearly defined. Here, we investigate the role of protein kinase C (PKC) in the mechanism of induction of IL-8 release by H. pylori in human gastric epithelial cells. In MKN45 cells, H. pylori-induced IL-8 release was enhanced by treatment with PKC inhibitors (GF109203X and calphostin C) and PKC depletion, which completely inhibited PKC activity. Moreover, PKC inhibitors and PKC depletion increased extracellular signal-regulated kinase (ERK) activity and phosphorylation, but not calcium / calmodulin-dependent protein kinase II (CaMK II) activity, in response to H. pylori infection. PKC activated by H. pylori inhibited activation of ERK induced by H. pylori without affecting the CaMK II activity and negatively regulated IL-8 production in human gastric epithelial cells.

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Stimulation of pepsinogen release from chief cells byHelicobacter pylori: evidence for a role of calcium and calmodulin

Cited by 3 publications

References 21 publications

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

Diabetes, insulin use and Helicobacter pylori eradication: a retrospective cohort study

Protein Kinase C Activation by Helicobacter pylori in Human Gastric Epithelial Cells Limits Interleukin-8 Production Through Suppression of Extracellular Signal-Regulated Kinase

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