Summary
The effect of 10 commercial lipopolysaccharides (LPS) and of 5 highly purified LPS
with variable but defined polysaccharide content, two LPS from anaerobic bacteria,
two mucopeptides and two meningococcal polysaccharides, was studied on rabbit and
human platelets. All the LPS preparations induced aggregation in rabbit heparinized
platelet-rich plasma (PRP) but to differing degrees. However, a preparation consisting
essentially of lipid A (from Salmonella minnesota Re 595) was one of the most active.
The mucopeptides were very potent whereas the meningococcal polysaccharides had no
effect. The activity was abolished by inactivation of complement. The lack of ability
of LPS and mucopeptides to aggregate rabbit platelets in ethyleneglycol tetraacetic
acid (EGTA) – PRP suggests that the mechanism depends on activation of the classical
pathway of complement. None of the bacterial products induced aggregation of human
platelets.
When washed rabbit platelets are mixed with complement-depleted rabbit serum and calcium
chloride, generation of thrombin occurs. Washed platelets contribute to thrombin generation
by providing factor V, a factor X activating activity, and possibly phospholipid (Brit.
J. Haemat. 36: 107, 1977). All the LPS preparations but not the mucopeptides or meningococcal
polysaccharides enhanced the rate of thrombin formation by enhancing the factor X
activating activity of rabbit or human platelets.
It is concluded that LPS affect rabbit platelets both by complement-dependent and
complement-independent mechanisms, but human platelets only by the complement- independent
pathway. Mucopeptides react with platelets only by the complement-dependent way and
have no effect on human platelets.
