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Malarial parasites, Plasmodium vinckei petteri, taken from lipopolysaccharide (LPS) high-responder (C3H/HeJGiFWeHi) mice which had been injected 7 to 8 h previously with either Escherichia coli LPS B or LPS W incorporated the purine nucleotide precursor hypoxanthine more slowly in an in vitro assay than parasites taken from saline-injected controls. In contrast, malarial parasites taken from LPS low-responder C3H/HeJ mice after injection of either LPS B or LPS W did not show reduced levels of hypoxanthine incorporation. These differing results with LPS high- and low-responder mouse strains demonstrated that the cytostatic effect on the parasites seen in the high-responder strain was not due to the direct action of LPS and implied that the cytostasis was mediated via host lymphoreticular cells. Furthermore, the failure of LPS B, a lipid A-associated protein-containing LPS preparation, to elicit a cytostatic effect on P. vinckei petteri in C3H/HeJ mice suggested that the LPS-induced effector mechanisms acting against malarial parasites may be similar to those reported against bacteria and tumors.

Failure of bacterial lipopolysaccharide to elicit a cytostatic effect on Plasmodium vinckei petteri in C3H/HeJ mice