{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T19:19:45Z","timestamp":1765653585485,"version":"3.48.0"},"reference-count":27,"publisher":"BMJ","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2002,1]]},"abstract":"<jats:p>\n                    Background: Different acid and peptic related gastroduodenal diseases are associated with both increased gastric secretion and\n                    <jats:italic>Helicobacter pylori<\/jats:italic>\n                    infection. Patients with\n                    <jats:italic>H pylori<\/jats:italic>\n                    associated gastritis or duodenal ulcer have increased serum pepsinogen levels which decrease after eradication. The mechanisms of\n                    <jats:italic>H pylori<\/jats:italic>\n                    induced gastric mucosal damage are not completely understood.\n                  <\/jats:p>\n                  <jats:p>\n                    Aim: To determine the effects of\n                    <jats:italic>H pylori<\/jats:italic>\n                    on pepsinogen secretion from isolated human peptic cells.\n                  <\/jats:p>\n                  <jats:p>\n                    Methods: Dispersed human peptic cells were prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and density gradient centrifugation.\n                    <jats:italic>H pylori<\/jats:italic>\n                    was obtained from gastric biopsies (antrum and body), and cultured in non-selective and selective media. Isolates of\n                    <jats:italic>H pylori<\/jats:italic>\n                    were used at different concentrations (1\u201320\u00d710\n                    <jats:sup>6<\/jats:sup>\n                    colony forming units (cfu)).\n                  <\/jats:p>\n                  <jats:p>\n                    Results:\n                    <jats:italic>H pylori<\/jats:italic>\n                    (10\n                    <jats:sup>6<\/jats:sup>\n                    \u20132\u00d710\n                    <jats:sup>7<\/jats:sup>\n                    cfu) increased basal pepsinogen secretion in a concentration dependent manner. This stimulus was not observed with\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    . The increased secretion was in addition to that observed with 0.1 mM histamine and 0.1 mM dibutyryl-cyclic adenosine monophosphate. However,\n                    <jats:italic>H pylori<\/jats:italic>\n                    did not affect either carbamylcholine (0.1\u201310 \u03bcM) or cholecystokinin (1 \u03bcM) stimulated pepsinogen secretion. Addition of the nitric oxide synthase inhibitor N\n                    <jats:sup>w<\/jats:sup>\n                    -monomethyl-\n                    <jats:sc>l<\/jats:sc>\n                    -arginine (1 mM) inhibited\n                    <jats:italic>H pylori<\/jats:italic>\n                    induced cGMP generation and pepsinogen secretion, which were also reduced in the absence of extracellular calcium.\n                    <jats:italic>H pylori<\/jats:italic>\n                    induced pepsinogen secretion was not affected by the absence\/presence of the\n                    <jats:italic>cagA<\/jats:italic>\n                    gene.\n                  <\/jats:p>\n                  <jats:p>\n                    Conclusions:\n                    <jats:italic>H pylori<\/jats:italic>\n                    increases pepsinogen secretion from human peptic cells through a calcium and nitric oxide mediated intracellular pathway. This effect is independent of the\n                    <jats:italic>H pylori<\/jats:italic>\n                    virulent\n                    <jats:italic>cagA<\/jats:italic>\n                    gene, and may be a mechanism of\n                    <jats:italic>H pylori<\/jats:italic>\n                    induced gastric mucosal damage.\n                  <\/jats:p>","DOI":"10.1136\/gut.50.1.13","type":"journal-article","created":{"date-parts":[[2002,7,27]],"date-time":"2002-07-27T06:29:07Z","timestamp":1027751347000},"page":"13-18","source":"Crossref","is-referenced-by-count":52,"title":["<i>Helicobacter pylori<\/i>\n                    stimulates pepsinogen secretion from isolated human peptic 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