thromboxane-b2 and Malaria

Peritoneal cells from mice infected with Plasmodium vinckei vinckei generate about four times more prostaglandin F and 6-keto prostaglandin F1 alpha, five times the prostaglandin E and ten times the thromboxane B2 than do peritoneal cells from normal mice. These results were not due to differences in the ratios of cell subpopulations from each group. As well as providing additional evidence that macrophage activation occurs in malaria, the increased production of these prostanoids could help explain some of the manifestations of this disease.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acids; Female; Leukocytes; Macrophage Activation; Macrophages; Malaria; Male; Mice; Mice, Inbred C57BL; Peritoneal Cavity; Prostaglandins E; Prostaglandins F; Thromboxane B2

Golden hamsters inoculated intraperitoneally with Plasmodium bergei infected mouse blood regularly developed P. bergei parasitaemia. This was associated with progressive thrombocytopenia and leucocytosis as the degree of parasitaemia increased with time. When infected whole blood was stimulated with collagen, significantly enhanced thromboxane B2 (TXB2) production per platelet was seen. 6-keto prostaglandin (PG) F1 alpha formation in the same system increased from the sixth infection day onwards and correlated with the relative leukocytosis. The production of 6-keto PGF1 alpha by aorta rings was significantly higher during the 4-7th days postinoculation. The increase in thromboxane production however was much more important than that of 6-keto PGF1 alpha and it therefore is concluded that P. bergei parasitaemia in hamsters tilts the haemostatic balance towards the platelet hyperaggregability that has also been described in P. falciparum infection in man.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Aorta; Blood Platelets; Cricetinae; Leukocyte Count; Leukocytes; Malaria; Mesocricetus; Mice; Mice, Inbred Strains; Plasmodium berghei; Thromboxane B2; Thromboxanes