Early and extensive CD55 loss from red blood cells supports a causal role in malarial anaemia
1 Mother-Offspring Malaria Studies Project, Muheza Designated District Hospital, Muheza, Tanzania
2 Sokoine University of Agriculture, Morogoro, Tanzania
3 Biomedical and Environmental Thematic Group, Ifakara Health Institute (IHI), PO Box 53, Ifakara, Tanzania
4 Seattle Biomedical Research Institute, Seattle, WA, USA
5 Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, NIH, Rockville, MD 20892, USA
6 Programs for Appropriate Technologies in Health (PATH), Seattle, WA 98121, USA
Malaria Journal 2011, 10:386 doi:10.1186/1475-2875-10-386Published: 29 December 2011
Levels of complement regulatory proteins (CrP) on the surface of red blood cells (RBC) decrease during severe malarial anaemia and as part of cell ageing process. It remains unclear whether CrP changes seen during malaria contribute to the development of anaemia, or result from an altered RBC age distribution due to suppressive effects of malaria on erythropoiesis.
A cross sectional study was conducted in the north-east coast of Tanzania to investigate whether the changes in glycosylphosphatidylinositol (GPI)-anchored complement regulatory proteins (CD55 and CD59) contributes to malaria anaemia. Blood samples were collected from a cohort of children under intensive surveillance for Plasmodium falciparum parasitaemia and illness. Levels of CD55 and CD59 were measured by flow cytometer and compared between anaemic (8.08 g/dl) and non- anaemic children (11.42 g/dl).
Levels of CD55 and CD59 decreased with increased RBC age. CD55 levels were lower in anaemic children and the difference was seen in RBC of all ages. Levels of CD59 were lower in anaemic children, but these differences were not significant. CD55, but not CD59, levels correlated positively with the level of haemoglobin in anaemic children.
The extent of CD55 loss from RBC of all ages early in the course of malarial anaemia and the correlation of CD55 with haemoglobin levels support the hypothesis that CD55 may play a causal role in this disorder.