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Mechanisms of Lipopolysaccharide-Initiated Rabbit Platelet Responses

II. Evidence That Lipid a Is Responsible for Binding of Lipopolysaccharide to the Platelet¹

From the Department of Immunopathology, Research Institute of Scripps Clinic, La Jolla, California 92037

Abstract

The mechanism of bacterial lipopolysaccharide- (LPS) initiated, complement- (C) mediated rabbit platelet lysis has been examined. The results of these studies support our previous observations that activation of the alternative C pathway is required for platelet lysis and that preparations of LPS that activate only the classical pathway (e.g., lipid A) do not cause lysis. The temporal relationship of the interaction of the LPS with the platelet before the addition of plasma suggests a time-dependent association of the LPS with the platelet. On the basis of a number of experiments, including inhibition with polymyxin B, treatment of LPS with alkali, and blocking experiments with polysaccharide-free LPS preparations, it is concluded that the lipid A region of the LPS molecule is responsible for attaching the LPS to the platelet. Finally, a comparison of the activity of lipid A-associated protein-LPS complexes with protein-free LPS demonstrated that an equivalent extent of platelet lysis was achieved with one-one hundredth the concentration of the former as that required for protein-free LPS. The data suggest that LAP facilitates attachment of the LPS to the platelet.

Footnotes

¹ This is publication Number 1489 from the Department of Immunopathology, Scripps Clinic and Research Foundation, 10666 North Torrey Pines Road, La Jolla, California. This research was supported by National Institutes of Health Grants AL-13187, NHLBI-16411, and Council for Tobacco Research Grant 764-E.

² Supported by United States Public Health Service Research Career Development Award 5K04 A1-00081.