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Blood, 1 February 2006, Vol. 107, No. 3, pp. 1192-1199.
Prepublished online as a Blood First Edition Paper on October 6, 2005; DOI 10.1182/blood-2005-08-3460.
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Submitted August 31, 2005
Accepted September 27, 2005
Severe malarial anemia of low parasite burden in rodent models results from accelerated clearance of uninfected erythrocytes
Krystal J Evans, Diana S Hansen, Nico van Rooijen, Lynn A Buckingham, and Louis Schofield*
The Walter and Eliza Hall Institute of Medical Research (WEHI), Parkville, VIC, Australia
Department of Molecular Cell Biology, Vrije Universiteit, Amsterdam, The Netherlands
* Corresponding author; email: schofield{at}wehi.edu.au.
Severe malarial anemia (SMA) is the most frequent life-threatening complication of malaria, and may contribute to the majority of malarial deaths worldwide. To explore the mechanisms of pathogenesis we developed a novel murine model of SMA in which parasitemias peaked around 1.0% of circulating red blood cells (RBCs) and yet hemoglobin (Hb) levels fell to 47-56% of baseline. The severity of anemia was independent of the level of peak or cumulative parasitemia, but was linked kinetically to the duration of patent infection. In vivo biotinylation analysis of the circulating blood compartment revealed that anemia arose from accelerated RBC turnover. Labelled RBCs were reduced to 1% of circulating cells by 8 days post-labelling, indicating that the entire blood compartment had been turned over in approximately one week. The survival rate of freshly transfused RBCs was also markedly reduced in SMA animals, but was not altered when RBCs from SMA donors were transferred into naive recipients, suggesting few functional modifications to target RBCs. Anemia was significantly alleviated by depletion of either phagocytic cells or CD4+ T lymphocytes. This study demonstrates that immunological mechanisms may contribute to SMA by promoting the accelerated turnover of uninfected RBCs.
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