The aim of this paper is to investigate the association of IL-8-251A/T polymorphism and Helicobacter pylori (H. pylori) infection with the risk of developing gastric cardiac adenocarcinoma (GCA) in the south of Taihang Mountain, a high-incidence area of esophageal cancer in China.
Relationship of IL-8 production and the CagA status in AGS cells infected with Helicobacter pylori exposed to low pH and activating transcription factor 3 (ATF3).
Enhanced gastric IL-18 mRNA expression in Helicobacter pylori-infected children is associated with macrophage infiltration, IL-8, and IL-1 beta mRNA expression.
SHXT and baicalin also inhibited Helicobacter pylori-induced inducible nitric oxide synthase (iNOS) and IL-8 mRNA expression, and decreased NO and IL-8 production.
Genetic polymorphisms of NOD1 and IL-8, but not polymorphisms of TLR4 genes, are associated with Helicobacter pylori-induced duodenal ulcer and gastritis.
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.
Helicobacter pylori strains possessing the cag pathogenicity island (PaI) are associated with the development of gastroduodenal diseases, including gastric cancer. cag PaI products induce the secretion of interleukin-8 (IL-8) from epithelial cells and facilitate the translocation of CagA into the cell cytosol.
Since oxygen radicals are considered as an important regulator in the pathogenesis of Helicobacter pylori (H. pylori)-induced gastric ulceration and carcinogenesis, chemokines such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) may be regulated by NF-kappaB and/or AP-1.
Isolates of Helicobacter pylori from dyspeptic patients in England and South Africa were tested for ability to induce interleukin-8 (IL-8) in gastric cells.
This study examined associations between anti-Helicobacter pylori immunoglobulin G antibody seropositivity and functional polymorphisms of interleukin-8 T-251 A and interleukin-10 T-819C.
Serum levels of anti-Hp and anti-CagA antibodies as well as IL-8 and TNF-alpha were measured by enzyme-linked immunosorbent assay (ELISA), while serum and tumor contents of progastrin and amidated gastrin were determined by specific RIA.
(1) GC patients have higher Hp and CagA seroprevalence than matched controls, confirming that CagA-positive Hp infection is associated with higher risk of GC; (2) serum levels of amidated gastrins and their precursor, progastrin, as well as IL-8 are significantly higher, while serum PG-I levels are reduced in intestinal type GC compared to controls, and (3) determination of high serum progastrin, amidated gastrins and IL-8 combined with low serum PG-I may be useful biomarkers of GC.
Increased gastric production of interleukin 8 and tumor necrosis factor alpha (TNF-alpha) has been implicated in the pathogenesis of Helicobacter pylori-associated gastroduodenal disease.
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.