Polysaccharide part of Proteus mirabilis lipopolysaccharide may be responsible for the stimulation of platelet adhesion to collagen.

Lipopolysaccharide (LPS, endotoxin) is a well-known causative agent of septic shock and disseminated intravascular coagulation. The action of LPS is related to the activation of many types of cells, including blood platelets. We examined the effects of different LPSs from Proteus mirabilis (smooth form LPS S1959 and rough forms LPSs R110 and R45) and fragments of LPS structure (lipid A and polysaccharide part) on platelet adhesion to collagen in the presence or absence of the phoinositide 3-kinase (PI 3-K) inhibitor, wortmannin. We found that all forms of LPS and its fragments caused the stimulation of platelet adhesion to collagen, but the polysaccharide part (PS S1959) was the most important in this action. Wortmannin had no effect on LPS-stimulated platelet adhesion to collagen. We conclude that both lipid A and PS S1959 play important roles in LPS-stimulated platelet adhesion to collagen independent on the PI 3-K action.