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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.
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Helicobacter pylori is a gram-negative, microaerophilic rod-shaped bacteria that lives beneath the gastric mucous layer, on the surface of epithelial cells. Stomach infection with this organism causes inflammation of the gastric mucosa, which can lead to gastritis, duodenal or gastric ulcer and even in rare cases to gastric carcinoma or MALT lymphoma. Approximately 50% of the world's population is believed to be infected with H. pylori. Most infections is probably acquired in childhood, but the exact route of transmission is unknown. It has been speculated that dental plaque might harbour Helicobacter pylori and, therefore, might be a source of gastric infection. In order to address this issue we studied the relationships between oral and gastric infections with H. pylori in 100 subjects. Methods: Gastric H. pylori infection was determined by 13C-urea breath test (UBT) and the presence of the bacteria in oral cavity was monitored by the culture from the saliva and from dental plaque. Results: H. pylori was found in the stomach in 51% of studied individuals, while oral H. pylori was found in 54% (in saliva) and in 48.3% (in gingival pockets), the difference was not statistical significant (p=NS). Interestingly, anti-Hp IgA was found in 84% of studied individuals. No relationship was found between the presence of the bacteria in the oral cavity and the H. pylori gastric infection. 54.9% of subjects with stomach infection showed concomitant presence of H. pylori in saliva. 53.2% of examined subjects with negative UBT-test revealed the presence of H. pylori in culture from the saliva. The X2 value of relationship between UBT and culture H pylori in saliva was 0.029 (p=0.9). Similarly, no relationship was found between the presence of H. pylori in the stomach and in the dental plaque (X2=0.6; p=0.4). As expected, the presence of H. pylori in the dental plaque was significantly correlated with the presence of bacteria in the saliva (X2=18.4; p=0.0002). We also compared the presence of H. pylori in the saliva of patients with and without teeth. The cultured H. pylori was found in 63.7% of patients without teeth and in 52.9% of patients with teeth. This indicates that the presence of teeth does not seem to affect the occurrence of H. pylori in saliva. We conclude that oral cavity contamination with of H. pylori occurs at similar degree to that in the stomach. However, there was no significant correlation between the occurrence of H. pylori in the stomach and in the oral cavity indicating that other factors, like susceptibility to infection due to acid environment in the stomach may be the major factor in gastric infection with that bacteria, while oral cavity may serve only as transient food-related contamination without clear relation to gastric infection.
The development of cancer is associated with high oxidative stress and at the same time with immune system activation. Tumors develop efficient mechanisms of protection against the immune response, which allow them to escape the immune surveillance. Simultaneously, key events in the process of carcinogenesis are related to oxidative stress. The relationship between the two remains unknown. Novel understanding of oxidative stress shows that discrete changes of activities of certain enzyme systems such as NADPH oxidases or nitric oxide synthases may be more important than the overall balance of production and removal of reactive oxygen species. Such imbalance of nitric oxide and superoxide production could modify inflammation and immune regulation. We studied superoxide anion production (by lucigenin enhanced chemiluminescence - 5 µM), NADPH oxidase activity and nitric oxide synthase (NOS) dysfunction. In parallel mRNA expression of immunomodulatory markers such as FoxP3 (T regulatory cell marker), CCR6 (mucosal homing effector T cell marker) and CD85j (NK cell/CD8 T cell Ig-like MHC class I inhibitory receptor) was determined. Basal superoxide production and NADPH oxidase activity are increased in oral squamous cell carcinoma. Tumor superoxide production was inhibited by NADPH oxidase inhibitor apocynin and by NOS inhibitor L-NAME. This indicates, for the first time, that oral squamous cell carcinoma is characterized by dysregulated nitric oxide synthase, which apart from increased NADPH oxidase activity contributes to oxidative stress and may be related to the immuno-pathology of these tumors. Studied tumors were infiltrated by CCR6+, but showed lower expression of both CD85j and FoxP3 mRNA. Finally, the CD85j mRNA expression was inversely correlated to oxidative stress parameters. These preliminary studies indicate that tumor oxidative stress, related to NADPH oxidase activity and NOS activity could be related to immune responses to cancer, thus therapeutic modification of oxidative stress, which could include the correction of NOS dysfunction, could facilitate immune surveillance.
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