نتایج جستجو برای: gastric epithelial cells helicobacter pylori
تعداد نتایج: 1535868 فیلتر نتایج به سال:
The mechanisms involved in mediating the enhanced gastric epithelial cell apoptosis observed during infection with Helicobacter pylori in vivo are unknown. To determine whether H. pylori directly induces apoptosis of gastric epithelial cells in vitro and to define the role of the Fas-Fas ligand signal transduction cascade, human gastric epithelial cells were infected with H. pylori for up to 72...
background helicobacter pylori (h. pylori) is recognized as the causative agent of peptic and duodenal ulcers, gastric adenocarcinoma, and low-grade mucosa-associated lymphoid tissue (malt) lymphoma . in the present study, we investigate the genotoxic damage of lysates of h. pylori in human b lymphocytes. materials and methodsâ human b lymphocytes were treated with 0, 10, 20, and 30 âµg/ l of ...
BACKGROUND Strains of Helicobacter pylori carrying the virulence associated cag pathogenicity island (PAI) induce gastric epithelial synthesis of the chemokine interleukin-8 (IL-8), a neutrophil chemoattractant, and thereby a strong inflammatory response during chronic infection of the human gastric mucosa. Previous mutational analyses have shown that many genes in the cag PAI are needed to eli...
Background—Strains of Helicobacter pylori carrying the virulence associated cag pathogenicity island (PAI) induce gastric epithelial synthesis of the chemokine interleukin-8 (IL-8), a neutrophil chemoattractant, and thereby a strong inflammatory response during chronic infection of the human gastric mucosa. Previous mutational analyses have shown that many genes in the cag PAI are needed to eli...
AIM Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimula...
no.: P03.07 CHARACTERIZATION OF NEW HUMAN GASTRIC EPITHELIAL CELL LINES DERIVED FROM NCI-N87 CELLS AFTER OVER-EXPRESSION OF HUMAN TELOMERASE CATALYTIC SUBUNIT K. D. Saraiva-Pava,* N. Navabi, S. Lindén, M. Oleastro and M. Roxo-Rosa* *Faculty of Engineering, Rio de Mouro, Portugal; Mucosal Immunobiology and Vaccine Center, Gothenburg University, Goteborg, Sweden; Departamento de Doenças Infeccios...
th most common malignant disease and the 3 rd leading cause of cancer death worldwide. Like most cancers, incidence increases with age. Unlike most other cancers a dominant environmental cause has been established, as chronic infection by Helicobacter pylori contributes about 90% of the attributable risk in " non-cardia " gastric cancer, the most common type globally [1]. The development of gas...
Helicobacter pylori infection is the strongest risk factor for development of gastric cancer. Host cellular stress responses, including inflammatory and immune responses, have been reported highly linked to H. pylori-induced carcinogenesis. However, whether mitochondrial regulation and metabolic reprogramming, which are potently associated with various cancers, play a role in H. pylori-induced ...
Helicobacter pylori (H. pylori) is considered to predispose carriers to gastric cancer but its role on gastric carcinogenesis is still unknown. The aim of this study was to investigate DNA damage by the comet assay in gastric epithelial cells from antrum and corpus in H. pylori-infected patients with gastritis of different degrees. H. pylori status, gastric histology, and DNA damage were studie...
Human Helicobacter pylori infection gives rise to an active chronic gastritis and is a major risk factor for the development of duodenal ulcer disease and gastric adenocarcinoma. The infection is accompanied by a large accumulation of immunoglobulin A (IgA)-secreting cells in the gastric mucosa, and following mucosal immunization only H. pylori-infected volunteers mounted a B-cell response in t...
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