Trypanossoma cruzi: course of infection in platelets-depleted mice

Abstract

The effect of platelet depletion on the course of Trypanosoma cruzi infection in BALB/c mice was investigated. Thrombocytopenia was achieved by inoculation of rabbit anti-platelet IgG during the parasitemic phase of the infection. The number of parasites in the blood of anti-platelet IgG treated was significantly higher than that of non-treated control mice, during the phase of high parasitemia. Cumulative mortality of platelet-depleted mice was consistently but not significantly higher than that of control mice up to the 32nd day of infection; from the 33rd day on they were equivalent, no mortalities occurring from then on, until observations were discontinued on the 60th day. These results suggest that platelets participate of the mechanisms of parasites removal from the bloodstream, but do not have an effective role in the mechanisms of defence against T. cruzi, during the acute phase of infection.

Trypanosoma cruzi-associated cerebrovascular disease: a case-control study in Eastern Colombia

“…Unfortunately, cerebral vascular autoregulation cannot counteract this vasoconstriction because autonomic dysfunction is also present in the majority of these patients perpetuating the condition with an intense and sustained vasoconstriction [15,18]. Hemorrhagic events seem to be less frequent in these cases and they might be the result of not only dysautonomic changes but of secondary haematologic abnormalities due to parasitic invasion of bone marrow or spleen [19].…”

Thromboxane A2 is a key regulator of pathogenesis during Trypanosoma cruzi infection

“…As such, TP expression is deleted in all cells. This results in defi cits in both platelet (30) and monocyte activation (11,31), both of which potently regulate parasite number (32)(33)(34). To dissect the role of TP on somatic cells versus cells engaged in innate immunity we transplanted BM cells into irradiated mice to repopulate the hematopoietic-derived cells and examined mortality after T. cruzi infection ( Fig.…”

Ginkgo biloba attenuated detrimental inflammatory and oxidative events due to Trypanosoma brucei rhodesiense in mice treated with melarsoprol

“…The thrombocytopenia observed during T.b.r infection could be attributed to damage to platelets by ROS [ 52 – 53 ]. Low platelet counts could also be attributable to the pooling of blood in the spleen, removal of platelets by the mononuclear phagocytic system and increased ‘consumption’ of platelets by disseminated intravascular coagulation reaction during trypanosomiasis infections [ 54 – 55 ].…”