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Cytokines and gastric inflammation in H.pylori infection

100%

Crabtree J. E.

nr 1

The relationship between the presence of Helicobacter pylori in the oral cavity and gastric in the stomach

84%

Loster B. W. , Majewski S. W. , Czesnikiewicz-Guzik M. , Bielanski W. , Pierzchalski P. , Konturek S. J.

tom 57

nr 3

91-100

There are numerous studies suggesting that inflammation of the oral cavity caused by bacteria or fungi is accompanied by gastric inflammation. This is particularly relevant in patients using complete dentures. Since the presence of H. pylori in the oral cavity can be easily discovered by bacteria culture and that in the stomach by 13C urea breath test (UBT) and histology of gastric endoscopic biopsy samples it is reasonably to state that the majority of the patients show the presence of bacterium in oral cavity and active gastric H. pylori infection. When comparing, however, the bacteria culture originating from the oral mucosa to those from the gastric mucosa, employing molecular biology examination, such as polymerase chain reaction (PCR), we found that the oral bacteria and those originating from stomach are completely different, suggesting that H. pylori may be present only transiently in oral cavity and does not play major role in gastric H. pylori infection. Thus, oral cavity does not serve as bacterial reservoir to infect gastric mucosa. Most important finding of our study is that patients with recognized inflammation in the oral cavity in the form of stomatitis prothetica hyperplasica both fibrosa as well as papillaris showed in nearly 100% gastric H. pylori infection, usually without the presence of the same bacterium in the oral cavity, suggesting that gastric H. pylori infection affects oral mucosa at distance by some, as yet, unknown mechanism.

15-deoxy-delta12,14-prostaglandin J2 suppresses RANTES expression by inhibiting NADPH oxidase activation in Helicobater pylori-infected gastric epithelial cells

67%

Cha B. , Lim J. W. , Kim K. H. , Kim H.

nr 2

Peroxisome proliferators-activated receptor-g (PPAR-g) is a ligand-activated transcription factor. 15 deoxy-12,14 prostaglandin J2 (15d-PGJ2) is a potent PPAR- ligand and acts as an anti-inflammatory agent via PPAR--dependent and independent mechanisms. Helicobacter pylori (H. pylori) induces gastric inflammation by inducing the activation of oxidant-sensitive transcription factor NF-B and cytokine expression in gastric epithelial cells. Since 15d-PGJ2 inhibits NF-B activation in various cells, it may suppress H. pylori-induced inflammatory signaling and cytokine expression in gastric epithelial cells. The present study aims to determined the effect of 15d-PGJ2 on the activation of inflammatory mediators Jak/Stat (Janus kinase/signal transducers and activators of transcription) and induction of cytokine RANTES in H. pylori-infected gastric epithelial AGS cells. Since NADPH oxidase is a candidate for the production of reactive oxygen species in H. pylori-infected gastric epithelial cells, we determined the effect of 15d-PGJ2 on the activation of NADPH oxdase. AGS cells were cultured in the presence of H. pylori treated with or without 15d-PGJ2. The activations of NADPH oxidase and Jak1/Stat3, the levels of H2O2 and RANTES in the medium, and DNA binding activity of Stat3 were assessed. A Jak/Stat3 specific inhibitor AG490 and an inhibitor of NADPH oxidase diphenyleneiodonium (DPI) were treated to determine the direct involvement of Jak/Stat and NADPH oxidase on the production of H2O2 and RANTES in H. pylori-infected cells. H. pylori induced the production of H2O2 and RANTES as well as the activations of NADPH oxidase and Jak1/Stat3, which were inhibited by the treatment of 15d-PGJ2. DPI suppressed H. pylori-induced alterations similar to 15d-PGJ2. However, AG490 had no effect on NADPH oxidase activation, but reduced the level of RANTES in the medium released from H. pylori-infected cells. Conclusion: NADPH oxidase activation is an upstream signaling of Jak1/Stat3 activation and induction of RANTES in H. pylori-infected AGS cells. 15d-PGJ2, inhibits the activations of NADPH oxidase and Jak1/Stat3 and RANTES expression, suggesting that 15d-PGJ2 may be beneficial for the treatment of H. pylori-induced gastric inflammation.