P-selectin binds to bacterial lipopolysaccharide.
Multiple organ failure associated with disseminated intravascular coagulation is a frequent complication in septic shock patients. Accumulation of platelets and neutrophils in the organs contributes to the manifestation of lipopolysaccharide (LPS)-induced organ failure. Although a direct interaction between LPS and platelets is well documented, the nature of the surface receptor for LPS on platelets is unknown. In this article we show that P-selectin is a receptor for LPS. The binding of LPS to P-selectin is independent of Ca2+, and is blocked by antibodies to P-selectin, lipid A and fucoidan. Platelets pre-treated with thrombin showed fourfold higher binding of fluorescein isothiocyanate (FITC)-conjugated LPS compared to untreated platelets and the binding of FITC-conjugated LPS to platelets was blocked in the presence of anti-P-selectin antibodies. It is likely that the binding of LPS via P-selectin on activated platelets or epithelium could have a significant role in the pathophysiology of organ failure in septic shock.
Malhotra
R
R
Glycobiology Research Unit, Glaxo-Wellcome Medicines Research Centre, Stevenage, GB. RM18326@ggr.co.uk
Priest
R
R
Foster
M R
MR
Bird
M I
MI
D001792:Blood Platelets / Q000378:metabolism; D006801:Humans; D008070:Lipopolysaccharides / Q000378:metabolism*; D009504:Neutrophils / Q000378:metabolism; D019007:P-Selectin / Q000737:chemistry / Q000378:metabolism*; D011485:Protein Binding; D012995:Solubility
D008070:Lipopolysaccharides; D019007:P-Selectin