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Dyserythropoiesis and severe anaemia associated with malaria correlate with deficient interleukin‐12 production
Author(s) -
K Mohan,
Mary M. Stevenson
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.01126.x
Subject(s) - erythropoiesis , plasmodium chabaudi , spleen , immunology , cytokine , malaria , ineffective erythropoiesis , bone marrow , biology , pathogenesis , in vitro , reticulocyte , anemia , medicine , parasitemia , plasmodium falciparum , messenger rna , gene , biochemistry
Complex cytokine interactions occur during blood‐stage malaria which offer a unique opportunity to study their influence on the pathogenesis of malarial anaemia. Plasmodium chabaudi AS susceptible A/J mice experience severe and fatal anaemia whereas resistant C57BL/6 (B6) mice survive following moderate anaemia. In this study we analysed the role of IL‐12 in erythropoiesis and tested whether the levels of IL‐12 produced in these mice correlated with the extent of anaemia. In vitro , IL‐12 significantly enhanced the numbers of erythroid burst (BFU‐E) and colony forming units (CFU‐E) in bone marrow and spleen cells from normal and day 7 infected A/J and B6 mice. Despite the presence of IL‐12 in vitro , the level of splenic erythropoiesis in infected A/J mice was significantly lower than in B6 mice. Moreover, sera from infected B6 mice, but not A/J mice, significantly up‐regulated erythropoiesis in vitro and this enhancement correlated with several fold higher levels of IL‐12 in the sera of B6 compared to A/J mice. Furthermore, the erythropoietic potentiating effect of sera from infected B6 mice was abrogated following depletion of IL‐12. Taken together, these findings suggest that defective IL‐12 production in A/J mice during the early course of infection may result in fatal anaemia.