Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells.

Lorente, S. ; Doiz, O. ; Serrano, M.T. ; Castillo, J. (Universidad de Zaragoza) ; Lanas, A. (Universidad de Zaragoza)

Resumen: 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.

Idioma: Inglés

DOI: 10.1136/gut.50.1.13

Año: 2002

Publicado en: GUT 50, 1 (2002), 13-8
ISSN: 0017-5749

Factor impacto JCR: 6.323 (2002)

Categ. JCR: GASTROENTEROLOGY & HEPATOLOGY rank: 3 / 45 = 0.067 (2002) - Q1 - T1

Tipo y forma: Article (Published version)

Área (Departamento): Área Microbiología (Dpto. Microb.Med.Pr.,Sal.Públ.)
Área (Departamento): Area Medicina (Dpto. Medicina, Psiqu. y Derm.)