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Relationship between Vac A toxin and ammonia in Helicobacter pylori-induced apoptosis in human gastric epithelial cells

100%
Chiozzi V., Mazzini G., Oldani A., Sciullo A., Ventura U., Romano M., Boquet P., Ricci V.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 3
23-30
VacA toxin is one of the most important virulence factors produced by H. pylori even though neither its role nor its action mechanisms are completely understood. First considered as a toxin inducing only cell vacuolation, VacA causes apoptosis of gastric epithelial cells by targeting mitochondria. A hotly debated question about VacA action is its relationship with ammonia, which is produced in vivo by H. pylori urease. While ammonia is strictly required for VacA-dependent vacuolation, its role in VacA-induced apoptosis is much less defined. This study was thus aimed to investigate the relationship between VacA toxin and ammonia in H. pylori-induced mitochondrial damage and apoptosis of human gastric epithelial cells in culture by means of flow cytometry. Our results show that, unlike cell vacuolation, in MKN 28 cells neither apoptosis nor dissipation of mitochondrial transmembrane potential induced by VacA require ammonia. Nevertheless, ammonia significantly potentiates both these VacA-induced effects, but independently of the swelling of VacA-containing endosomes (i.e., vacuolation). Our findings make unlikely the hypothesis that ammonia-dependent swelling and rupture of endosomal vesicles in which VacA is sequestered after cell internalization may allow the toxin to reach mitochondria and trigger apoptosis.
2
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Helicobacter pylori in the oral cavity and its implications in gastric infection, periodontal health, immunology and dyspepsia

80%
Czesnikiewicz-Guzik M., Bielanski W., Guzik T. J., Loster B., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
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2005
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tom 56
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nr 6
77-89
Helicobacter pylori (H. pylori) is an important gastrointestinal pathogen associated with gastritis as well as gastric or duodenal ulcers and gastric cancer. The oral cavity has been considered as a potential reservoir for the gastric infection and reinfection. The objective of our studies was to evaluate the influence of oral H. pylori for the stomach infection and the release of gut hormones affecting food intake such as ghrelin and gastric secretion such as gastrin. Additionally, the contribution of H. pylori in the periodontal disease has been examined. H. pylori infection in stomach was assessed by 13C- Urease Breath Test and presence of the bacteria in oral cavity by culture. The periodontal status was measured by pockets depth with the periodontal probe. We estimated the serum level of IgG anti-H. pylori, anti-VacA, anti-CagA, ghrelin, gastrin, TNF-alpha and IL-8 in blood and the level of IgA anti-H. pylori in saliva. The presence of H. pylori in oral cavity was detected in 54.1% of examined individuals, whereas the H. pylori gastric infection in tested group was found in 51% cases. However, the correlation analysis between those two groups of patients involving together about 100 subjects showed that within the group of patients with positive gastric H. pylori infection only 45.1% did not show the presence of H. pylori in saliva and 43.1% showed no H. pylori in supragingival plaque. In line of these findings patients who did not have gastric H. pylori infection, 53.2 % showed presence of H. pylori in saliva and 42.9% in supragingival plaques. Serum level of ghrelin and gastrin in subjects with oral H. pylori inoculation but without gastric H. pylori infection were not significantly different from those without the presence of this germ in oral cavity. In contrast, gastric H. pylori infection resulted in significant reduction in serum ghrelin levels and significant elevation of gastrin as compared to those who were gastric H. pylori negative. We concluded that oral H. pylori alone does not seem to serve as bacterium sanctuary for gastric H. pylori infection and, unlike gastric infection, it fails to affect serum levels of hormones stimulating appetitive behaviour such as ghrelin and gastric acid secretion such as gastrin.
3
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Prevalence and characterization of Helicobacter pylori [H. pylori] infection and colonization in dentists

80%
Loster B. W., Czesnikiewicz-Guzik M., Bielanski W., Karczewska E., Loster J. E., Kalukin J., Guzik T. J., Majewski S., Konturek S. J.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 8
13-18
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