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    <subfield code="2">doi</subfield>
    <subfield code="a">10.1136/gut.50.1.13</subfield>
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  <datafield tag="024" ind1="8" ind2=" ">
    <subfield code="2">sideral</subfield>
    <subfield code="a">51932</subfield>
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  <datafield tag="037" ind1=" " ind2=" ">
    <subfield code="a">ART-2002-51932</subfield>
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  <datafield tag="041" ind1=" " ind2=" ">
    <subfield code="a">eng</subfield>
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  <datafield tag="100" ind1=" " ind2=" ">
    <subfield code="a">Lorente,  S.</subfield>
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  <datafield tag="245" ind1=" " ind2=" ">
    <subfield code="a">Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells.</subfield>
  </datafield>
  <datafield tag="260" ind1=" " ind2=" ">
    <subfield code="c">2002</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
    <subfield code="a">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 (1–20×106 colony forming units (cfu)).

Results: H pylori (106–2×107 cfu) increased basal pepsinogen secretion in a concentration dependent manner. This stimulus was not observed with Escherichia coli. The increased secretion was in addition to that observed with 0.1 mM histamine and 0.1 mM dibutyryl-cyclic adenosine monophosphate. However, H pylori did not affect either carbamylcholine (0.1–10 μM) or cholecystokinin (1 μM) stimulated pepsinogen secretion. Addition of the nitric oxide synthase inhibitor Nw-monomethyl-L-arginine (1 mM) inhibited H pylori induced cGMP generation and pepsinogen secretion, which were also reduced in the absence of extracellular calcium. H pylori induced pepsinogen secretion was not affected by the absence/presence of the cagA gene.

Conclusions: H pylori increases pepsinogen secretion from human peptic cells through a calcium and nitric oxide mediated intracellular pathway. This effect is independent of the H pylori virulent cagA gene, and may be a mechanism of H pylori induced gastric mucosal damage.</subfield>
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    <subfield code="9">info:eu-repo/semantics/closedAccess</subfield>
    <subfield code="a">All rights reserved</subfield>
    <subfield code="u">http://www.europeana.eu/rights/rr-f/</subfield>
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  <datafield tag="590" ind1=" " ind2=" ">
    <subfield code="a">6.323</subfield>
    <subfield code="b">2002</subfield>
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  <datafield tag="591" ind1=" " ind2=" ">
    <subfield code="a">GASTROENTEROLOGY &amp; HEPATOLOGY</subfield>
    <subfield code="b">3 / 45 = 0.067</subfield>
    <subfield code="c">2002</subfield>
    <subfield code="d">Q1</subfield>
    <subfield code="e">T1</subfield>
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    <subfield code="a">info:eu-repo/semantics/article</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Doiz,  O.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Serrano,  M.T.</subfield>
    <subfield code="0">(orcid)0000-0002-7119-2244</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Castillo,  J.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0002-2519-701X</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Lanas,  A.</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0001-5932-2889</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1008</subfield>
    <subfield code="2">630</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Microb.Med.Pr.,Sal.Públ.</subfield>
    <subfield code="c">Área Microbiología</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1007</subfield>
    <subfield code="2">610</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Medicina, Psiqu. y Derm.</subfield>
    <subfield code="c">Area Medicina</subfield>
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  <datafield tag="773" ind1=" " ind2=" ">
    <subfield code="g">50, 1 (2002), 13-8</subfield>
    <subfield code="p">Gut</subfield>
    <subfield code="t">GUT</subfield>
    <subfield code="x">0017-5749</subfield>
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    <subfield code="s">387300</subfield>
    <subfield code="u">http://zaguan.unizar.es/record/130275/files/texto_completo.pdf</subfield>
    <subfield code="y">Versión publicada</subfield>
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    <subfield code="a">2024-01-24-14:59:03</subfield>
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