We conclude that Hp promotes apoptosis in adenocarcinoma gastric epithelial cells in vitro and this is associated with activation of COX-2 and inhibition of HSP70.
Two virulence factors encoded by the cytotoxin-associated (cagA) gene and the vacuolating toxin (vacA) gene of Helicobacter pylori are known to be associated with gastroduodenal pathologic conditions.
Since HP infection is usually accompanied by an increase in plasma level of gastrin, which is also recognized as a trophic hormone for the colonic epithelium and a potent mitogen capable to induce cyclooxygenase-2 (COX-2), we decided 1) to compare the seroprevalence of HP, its cytotoxic protein, CagA, and cytokines (TNFalpha, IL-1beta and IL-8) in colorectal cancer patients, before and after removal of cancer, with those in age- and gender-matched controls; 2) to determine the gene expression of gastrin and gastrin receptors (CCK(B)-R) in colorectal cancer tissue, 3) to assess the plasma levels and tumor tissue contents of gastrin, 4) to examine the mRNA expression of cyclooxygenase COX-1 and COX-2 cancer tissue and intact colonic mucosa.
To determine the concentrations of leptin in plasma and gastric fundic mucosa in humans, with reference to Helicobacter pylori (H pylori) infection, and their association with gastric mucosal levels of interleukin (IL)-1beta, IL-6 and IL-8.
Hp GE-driven enhancement of lymphocyte cytotoxic activity was associated with the expansion of CD3(-)CD56(+)CD25(+) NK cells and the up-regulation of IFN-γ and/or IL-2 synthesis, up to the higher level in Hp(-) than in Hp(+), while Hp LPS-mediated decrease in lymphocyte cytotoxicity was accompanied by the lack of CD3(-)CD56(+)CD25(+) NK propagation, the inhibition of pro-inflammatory cytokine expression and intense expansion of IL-10-producing NK cells.
In the multivariate analysis, increasing serum gastrin levels (OR= 1.02; 95% CI= 1.01-1.12), increasing age (OR= 1.05; 95% CI= 1.02 - 1.09) and HP-positive status (OR = 2.88; 95% CI = 1.10 - 7.51) remained independently associated with CD.
The CagA protein is one of the virulence factors of Helicobacter pylori, and two major subtypes of CagA have been observed, the Western and East Asian type.
Highly virulent Helicobacter pylori cause proinflammatory signaling inducing the transcriptional activation and secretion of cytokines such as IL-8 in epithelial cells.
The aim of our study was to investigate the impact of interleukin (IL)-6 190C/T, IL-6174G/C, IL-6 572G/C, tumor necrosis factor-alpha (TNF-α) 308G/A, and angiotensin-converting enzyme (ACE) I/D gene polymorphisms on Helicobacter pylori (H. pylori) infection in children.A cross-sectional study was performed on 126 children (57 children with H. pylori infection and 69 children without H. pylori infection) aged between 3 and 18 years presenting to a Pediatrics Tertiary Hospital from Romania.
Short-term 8-week celecoxib, a selective COX-2 inhibitor, exerts a preliminary hint to improve regression in part for persistent IM after Helicobacter pylori eradication.
The aim of the study was to investigate if Lotus tetragonolobus and Maackia amurensis lectins influence the level of MUC1, MUC5AC, Lewis b, H type 1, sialyl Lewis x, phospho-IκBα and interleukin 8 in Helicobacter pylori infected gastric cancer cells.
The carcinogenic features of TNF-α are described in this review, and the TNF-α inducing protein (Tipα) of Helicobacter pylori genome is presented as an example of a tumor promoter of human stomach cancer development.
Plasma levels of cholesterol, LDL-cholesterol and fibrinogen as well as IL-8 were significantly higher in Hp positive subjects, especially in pts with ischemic stroke.
We conclude that Hp promotes apoptosis in adenocarcinoma gastric epithelial cells in vitro and this is associated with activation of COX-2 and inhibition of HSP70.
TNF-α-inducing protein of Helicobacter pylori induces epithelial-mesenchymal transition (EMT) in gastric cancer cells through activation of IL-6/STAT3 signaling pathway.