Plasmodium chabaudi AS: Erythropoietic responses during infection in resistant and susceptible mice
References (34)
- et al.
Why do some African children develop severe malaria
Parasitology Today
(1991) - et al.
Plasmodium berghei: Lactic acidosis and hypoglycaemia in a rodent model of severe malaria; effects of glucose, quinine and dichloroacetate
Experimental Parasitology
(1991) Erythropoietin
Blood
(1991)- et al.
Changes in hemopoietic stem cells in bone marrow of mice with Plasmodium berghei malaria
Blood
(1985) - et al.
The pathophysiology of severe falciparum malaria
Parasitology Today
(1986) - et al.
Murine malaria decreases hemopoietic stem cells
Blood
(1987) - et al.
Dependence on cell-mediated mechanisms for the appearance of crisis forms during Plasmodium chabaudi AS infection in C57BL/6 mice
Microbial Pathogenesis
(1990) - et al.
Changes in hemopoietic cell and regulator levels in mice during fatal or nonfatal malarial infections. 1. Erythropoietic populations
Experimental Parasitology
(1990) - et al.
Spleen stromal cell lines selectively support erythroid colony formation
Blood
(1989) - et al.
Muramyl dipeptide induces production of hemopoietic growth factors in vivo by a mechanism independent of tumor necrosis factor
Journal of Immunology
(1990)
Ineffective erythropoiesis in acute human falciparum malaria
Blut
Endotoxin-induced shunting of erythropoiesis in mice
American Journal of Physiology
Effective recovery and immunity to virulent malaria following red cell transfusions at crisis
Erythroid colony formation in cultures of mouse and human bone marrow: Analysis of the requirement for erythropoietin by gel filtration and affinity chromatography on agarose-concanavalin A
Journal of Cellular Physiology
Murine spleen culture: homing of hemopoietic progenitor cells to spleen is not mediated by a similar mechanism to that in marrow
Experimental Hematology
A simple microassay for erythropoietin based on [3H]thymidine incorporation into spleen cells from phenylhydrazine treated mice
Experimental Hematology
Reduced erythrocyte survival following clearance of malarial parasitemia in Thai patients
British Journal of Hematology
Cited by (61)
Bisphosphoglycerate Mutase Deficiency Protects against Cerebral Malaria and Severe Malaria-Induced Anemia
2020, Cell ReportsCitation Excerpt :These results suggest a more robust erythroid response in BpgmL166P mutants compared to controls following a purely hemolytic infection with PcA. Our data are in agreement with the reported critical importance of splenic stress erythropoiesis to the outcome of malaria (Weiss et al., 1989; Yap and Stevenson, 1992). The results demonstrate that the BpgmL166P mutation confers protection against both blood stage and CM in mouse models of these diseases, linked in part to the superior erythroid response of the mutant.
Adenosine monophosphate deaminase 3 activation shortens erythrocyte half-life and provides malaria resistance in mice
2016, BloodCitation Excerpt :This was further supported by the observation that human RBCs with artificially elevated GTP levels supported normal growth of Plasmodium falciparum (supplemental Figure 9). Mice carrying the Ampd3T689A allele exhibit splenomegaly, which is positively correlated with malaria resistance.32,33 Therefore, it is possible that the spleen mediates malaria resistance in the Ampd3T689A line.
Plasmodium berghei: Parasite clearance after treatment with dihydroartemisinin in an asplenic murine malaria model
2008, Experimental ParasitologyMalarial anemia: Of mice and men
2007, BloodCitation Excerpt :In contrast to the human studies cited, a decrease in mouse bone marrow cellularity of between 40% to 75% of normal levels is seen at peak parasitemia or death, whichever is reached first,62–65 with reductions in cellularity proportional to the severity of infection.54,63,66 However, despite these discrepancies with the reported pathology in human infection, reports of only a minimal reduction in the total number of BFU-Es, and at best only a modest increase in CFU-Es in mice,63–66 suggest that the bone marrow is unable to compensate for RBC loss in both humans and mice through increased erythropoiesis during the acute phase of infection. At present there are no studies reporting the production of dyserythropoietic erythroblasts during mouse malaria infection, most probably because there are few chronic infection models.
Pyruvate kinase deficiency: Correlation between enzyme activity, extent of hemolytic anemia and protection against malaria in independent mouse mutants
2007, Blood Cells, Molecules, and Diseases