thromboplastin and Helicobacter-Infections

Topics: Apoptosis; Cytokines; Helicobacter Infections; Helicobacter pylori; Humans; Lipid Peroxidation; Multiple Sclerosis; Platelet Aggregation; Reactive Oxygen Species; Scleroderma, Systemic; Thromboplastin

Different Helicobacter pylori lipopolysaccharides (LPSs) and LPS-derivatives were studied for their ability to induce the production of procoagulant activity (PCA) and plasminogen activator inhibitor type 2 (PAI-2) by human blood mononuclear leukocytes. Smooth (S)- and rough (R)-form LPSs caused a similar increase in cell-associated PCA (tissue factor) and PAI-2 antigen release. Both effects were potentiated by fetal bovine serum via a CD14-mediated mechanism. The potency of H. pylori LPSs was approximately 1000-fold lower than that of Salmonella typhimurium LPSs. When H. pylori LPS derivatives (dephosphorylated R-LPS, S-lipid A, and R-lipid A) were used, PCA and PAI-2 production were markedly reduced. R-lipid A was approximately 4-fold less efficient than S-lipid A. These findings suggest that the induction of monocyte tissue factor and PAI-2 by H. pylori LPS is influenced by the lipid A structure and modulated by the core oligosaccharide and that phosphate groups present in both regions may play an important role.

Topics: Helicobacter Infections; Helicobacter pylori; Humans; Leukocytes, Mononuclear; Lipopolysaccharide Receptors; Lipopolysaccharides; Plasminogen Activator Inhibitor 2; Salmonella typhimurium; Serum Albumin, Bovine; Thromboplastin