Research
Alterations on peripheral B cell subsets following an acute uncomplicated clinical malaria infection in children
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* Corresponding author: Rosemary Rochford rochforr@upstate.edu
1 School of Pure and Applied Science, Kenyatta University, Nairobi, Kenya
2 Kenya Medical Research Institute, Center for Global Health Research, Kisumu, Kenya
3 Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH, USA
4 Center for Outcomes Research and Evaluation, SUNY Upstate Medical University, Syracuse, NY, USA
5 Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, NY, USA
6 Biostatistics Lab, Human Adaptation and Countermeasures Division, National Aeronautics and Space Administration, Houston, TX, USA
Malaria Journal 2008, 7:238 doi:10.1186/1475-2875-7-238
Published: 18 November 2008Abstract
Background
The effects of Plasmodium falciparum on B-cell homeostasis have not been well characterized. This study investigated whether an episode of acute malaria in young children results in changes in the peripheral B cell phenotype.
Methods
Using flow-cytofluorimetric analysis, the B cell phenotypes found in the peripheral blood of children aged 2–5 years were characterized during an episode of acute uncomplicated clinical malaria and four weeks post-recovery and in healthy age-matched controls.
Results
There was a significant decrease in CD19+ B lymphocytes during acute malaria. Characterization of the CD19+ B cell subsets in the peripheral blood based on expression of IgD and CD38 revealed a significant decrease in the numbers of naive 1 CD38-IgD+ B cells while there was an increase in CD38+IgD- memory 3 B cells during acute malaria. Further analysis of the peripheral B cell phenotype also identified an expansion of transitional CD10+CD19+ B cells in children following an episode of acute malaria with up to 25% of total CD19+ B cell pool residing in this subset.
Conclusion
Children experiencing an episode of acute uncomplicated clinical malaria experienced profound disturbances in B cell homeostasis.