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 ~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 ~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.
|Number of pages||6|
|Journal||Journal of Infectious Diseases|
|Publication status||Published - 1996|
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health