Effect of helicobacter pylori lipopolysaccharide (lps) and lps derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells
Semeraro, N. Montemurro, P. Piccoli, C. Muoio, V. Colucci, M. Giuliani, G. Fumarola, D. Pece, S. Moran, A. P.
Semeraro, N.
Montemurro, P.
Piccoli, C.
Muoio, V.
Colucci, M.
Giuliani, G.
Fumarola, D.
Pece, S.
Moran, A. P.
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Date
1996-12-01
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journal article
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Citation
Semeraro, N. Montemurro, P.; Piccoli, C.; Muoio, V.; Colucci, M.; Giuliani, G.; Fumarola, D.; Pece, S.; Moran, A. P. (1996). Effect of helicobacter pylori lipopolysaccharide (lps) and lps derivatives on the production of tissue factor and plasminogen activator inhibitor type 2 by human blood mononuclear cells. Journal of Infectious Diseases 174 (6), 1255-1260
Abstract
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 similar to 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 similar to 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.
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Oxford University Press (OUP)