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Malaria toxins from P. chabaudi chabaudi AS and P. berghei ANKA cause dyserythropoiesis in C57BL/6 mice

Published online by Cambridge University Press:  01 November 1997

W. RUDIN
Affiliation:
Swiss Tropical Institute, PO Box, 4002 Basel, Switzerland
V. QUESNIAUX
Affiliation:
NOVARTIS AG, PO Box, 4002 Basel, Switzerland
N. FAVRE
Affiliation:
Swiss Tropical Institute, PO Box, 4002 Basel, Switzerland
G. BORDMANN
Affiliation:
Swiss Tropical Institute, PO Box, 4002 Basel, Switzerland

Abstract

The lack of correlation between parasitaemia and anaemia in severe malaria indicates that factors in addition to schizont rupture or erythrophagocytosis contribute to anaemia. We asked whether malaria toxin (MT) from Plasmodium berghei or P. chabaudi might impair erythropoiesis. Daily intraperitoneal injection of MT into C57BL/6 mice induced a transient reduction of RBC values by 25–30% after about 2 weeks, followed by increased haematopoiesis in the spleen as compared to mice receiving uninfected RBC preparations. There was a 3 (P. berghei) to 8-fold (P. chabaudi) increase of total proliferative activity in the spleen. Flow cytometric analyses showed that this was accompanied by some differentiation of TER-119 positive erythroid cells and of Gr-1 positive myeloid cells. Erythroid and myeloid progenitor cell-derived colony assays confirmed these results and revealed an increase in the number of CFU-E ([les ]200-fold), BFU-E ([les ]10-fold) and CFU-GM ([les ]20-fold) in the spleen of MT treated mice, as compared to controls.

Type
Research Article
Copyright
1997 Cambridge University Press

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