1,720,973 research outputs found
VacA release by H pylori: quantitation and vacuolating activity of free-soluble and outer membrane vesicle-associated toxin.
No full textRelationship between VacA toxin and ammonia in Helicobacter pylori-induced apoptosis in epithelial cells.
No full textIn memoriam of the gastric mucosal barrier: intracellular, intercellular and stromal invasion of human gastric mucosa by Helicobacter pylori.
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Helicobacter pylori vacuolating toxin accumulates within the endosomal-vacuolar compartment of cultured gastric cells and potentiates the vacuolating activity of ammonia
No full textGuanidine transport across the apical and basolateral membranes of human intestinal Caco-2 cells is mediated by two different mechanisms
No full textThe functional characteristics of the intestinal absorption and secretion of guanidine as a model
of a nutritionally and metabolically essential organic cation were examined in the Caco-2 human intestinal cell
line. Both apical and basolateral transport of [14C]-guanidine were studied using Caco-2 cells grown on polycarbonate
permeable membranes. The basolateral-to-apical flux of [14C]-guanidine (i.e., its secretion) was quantitatively
higher than the apical-to-basolateral transport (i.e., its absorption). When Na was replaced by K or Li,
both apical and basolateral accumulation were significantly inhibited. Studies using the cell monolayers and apical
membrane vesicles obtained from Caco-2 cells showed a potential-independent mechanism of guanidine apical
uptake and efflux. Conversely, basolateral uptake and efflux were membrane potential dependent. Kinetic analysis
revealed that both saturable and nonsaturable mechanisms accounted for the apical and basolateral accumulations.
The [14C]-guanidine efflux from cells through the apical and basolateral membranes was significantly
reduced at 4°C, suggesting carrier-mediated mechanisms. Moreover, the apical efflux was stimulated by an
inwardly directed H gradient. Influx and efflux of [14C]-guanidine were unaffected by the presence of tetraethylammonium,
cimetidine or decynium-22 in the donor compartment. Only quinine significantly reduced [14C]-
guanidine entrance through apical and basolateral membranes and its exit through the basolateral membrane. In
conclusion, our results suggest that the influx and the efflux through the apical membrane is mediated by different
transporters, whereas transport across the basolateral membrane is mediated by a member of the organic cation
transporter family with high affinity for guanidine
Significance of ammonia in the genesis of gastric epithelial lesions induced by Helicobacter pylori : An in vitro study with different bacterial strains and urea concentrations
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