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Prepublished online as a Blood First Edition Paper on March 20, 2003; DOI 10.1182/blood-2002-08-2437.
Submitted August 8, 2002
Accepted March 12, 2003
Accelerated senescence of human erythrocytes cultured with Plasmodium falciparum
Maria Fausta Omodeo-Sale*, Anna Motti, Nicoletta Basilico, Silvia Parapini, Piero Olliaro, and Donatella Taramelli
Istituto di Fisiologia Generale e Chimica Biologica Giovanni Esposito, Universita di Milano, Milano, Italy
Istituto di Microbiologia, Universita di Milano, Milano, Italy
UNDP/WB/WHO, Geneva, Switzerland
* Corresponding author; email: omodeo{at}mailserver.unimi.it.
Red blood cells infected with Plasmodium falciparum (IRBCs) undergo changes primarily in their membrane composition which contribute to malaria pathogenesis. However, all manifestations (e.g. anemia) cannot be accounted for by IRBCs alone. Uninfected erythrocytes (URBCs) may play a role, but have been under-researched. We wanted to document changes in the erythrocyte membrane that could contribute to URBC reduced lifespan and malaria-associated anemia. Human erythrocytes were cultured with P.falciparum, washed at the trophozoite stage, and IRBCs and URBCs were separated by centrifugation on Percoll density gradient, thus obtaining erythrocyte fractions of different densities/ages. IRBC and URBC purified membranes were analyzed and compared to control normal erythrocytes (NRBCs) of the same age, from the same donor, kept in the same conditions. P. falciparum accelerated aging of both IRBCs and URBCs, causing a significant increase of the most dense (old) fraction. Protein, phospholipid and cholesterol content were reduced in IRBCs and young URBCs. Compared to NRBCs, the young and medium uninfected fractions had higher levels of lipid peroxidation and phospholipid saturation (due to the loss of polyunsaturated fatty acids, PUFA) and lower phosphatidylserine. In IRBCs, thiobarbituric reactive substances (TBARS) were higher and PUFA and phosphatidylserine lower than NRBCs and URBCs. In comparison, trophozoite membranes had lower phospholipid (particularly sphingomyelin and phosphatidylserine) and cholesterol content, and a higher degree of saturation. Parasite-induced peroxidative damage might account for these modifications. In summary, we demonstrated that P. falciparum induces membrane changes associated with accelerated senescence in both infected and uninfected erythrocytes.URBCs will then likely contribute to malaria anemia (they are recognized as senescent and removed) and to organ damage (they aggravate congestion in small vessels).
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