Relative concentratiions of endotoxin-binding proteins in body fluids in children during infection

The serum protein lipopolysaccharide-binding protein [LBP] binds to the lipid A component of bacterial endotoxin and facilitates its delivery to the CD 14 antigen on the macrophages, where proinflammatory cytokines are released and a cascade of host mediators is initiated. The neutrophil granular protein bactericidal/permeability-increasing protein [BPI] competes with LBP for endotoxin binding and functions as a molecular antagonist of LBP-endotoxin interactions. We have measured concentrations of BPI and LBP in abscess cavities, enclosed infected body fluids, and non-infected body fluids from 36 children whose age ranged between 2 to 12 years [21 males and 15 females]. The mean values +/- SD of BPI/LBP in different body fluids were 12.12 +/- 5.11 in abscess cavities, 0.778 +/- 0.104 in infected body fluids, and 0.022 0.0624 in non-infected body fluids. The differences in BPI/LBP ratio between the three types of body fluids were highly significant [P<0.0001]. The mean BPI concentrations was higher in the 8 abscess cavities that contained gram negative organisms than in the 8 with gram positive or no organisms [P<0.005]. BPI concentrations were directly correlated with the quantity of neutrophils within abscess fluids [r[s] = 0.844, P< 0.001] and in infected body fluids [r[s] = 0.484, P<0.05]. In conclusion, BPI is available in sufficient quantities within abscess cavities for effective competition with LBP for endotoxin. BPI may attenuate the local inflammatory response and the systemic toxicity of endotoxin release during gram-negative infections

Surface and total tissue factor activity of endothelial cells.

With a technic that was developed by us, we found that normal human umbilical vein endothelial cells (HUVEC) in culture characteristically had very little tissue factor (TF) activity either on the surface or in the cells which had been disrupted. In the presence of endotoxin (E. coli O26:B6), a trigger for thrombosis in septicemic patients, we could not detect an increased TF activity of HUVEC on its surface. However, an increase in TF (total TF) was detected after disruption of the cells. The increase in total TF was dose-dependent. Endotoxin at the concentration of 10 micrograms/ml caused around 5 fold increase in total TF activity compared to that of HUVEC in the absence of endotoxin.