TY - JOUR
T1 - The levels of CD16/Fcγ receptor IIIA on CD14+ CD16 + monocytes are higher in children with severe Plasmodium falciparum anemia than in children with cerebral or uncomplicated malaria
AU - Ogonda, Lilian A.
AU - Orago, Alloys S.S.
AU - Otieno, Michael F.
AU - Adhiambo, Christine
AU - Otieno, Walter
AU - Stoute, José A.
PY - 2010/5
Y1 - 2010/5
N2 - Fc gamma receptor IIIA (CD16/FcγRIIIA) on monocytes/macrophages may play an important role in the pathogenesis of severe malarial anemia (SMA) by promoting phagocytosis of IgG-coated uninfected red cells and by allowing the production of tumor necrosis factor alpha (TNF-α) upon cross-linking by immune complexes (ICs). However, not much is known about the differential expression of this receptor on monocytes of children with severe malaria and uncomplicated malaria. Therefore, we investigated the expression of CD16/FcγRIIIA on monocytes of children with SMA, cerebral malaria (CM), and their age-matched uncomplicated malaria controls by flow cytometry. Since CD14low (CD14+) monocytes are considered more mature and macrophage-like than CD14high (CD14++) monocytes, we also compared the level of expression of CD16/FcγRIIIA according to the CD14 level and studied the relationship between CD16/FcγRIIIA expression and intracellular TNF-α production upon stimulation by ICs. CD16/FcγRIIIA expression was the highest overall on CD14+ CD16+ monocytes of children with SMA at enrollment. At convalescence, SMA children were the only ones to show a significant decline in the same parameter. In contrast, there were no significant differences among groups in the expression of CD16/FcγRIIIA on CD14++ CD16+ monocytes. A greater percentage of CD14+ CD16+ monocytes produced TNF-α upon stimulation than any other monocyte subset, and the amount of intracellular TNF-α correlated positively with CD16/FcγRIIIA expression. Furthermore, there was an inverse correlation between hemoglobin levels and CD16/FcγRIIIA expression in children with SMA and their controls. These data suggest that monocytes of children with SMA respond differently to Plasmodium falciparum infection by overexpressing CD16/FcγRIIIA as they mature, which could enhance erythrophagocytosis and TNF-α production.
AB - Fc gamma receptor IIIA (CD16/FcγRIIIA) on monocytes/macrophages may play an important role in the pathogenesis of severe malarial anemia (SMA) by promoting phagocytosis of IgG-coated uninfected red cells and by allowing the production of tumor necrosis factor alpha (TNF-α) upon cross-linking by immune complexes (ICs). However, not much is known about the differential expression of this receptor on monocytes of children with severe malaria and uncomplicated malaria. Therefore, we investigated the expression of CD16/FcγRIIIA on monocytes of children with SMA, cerebral malaria (CM), and their age-matched uncomplicated malaria controls by flow cytometry. Since CD14low (CD14+) monocytes are considered more mature and macrophage-like than CD14high (CD14++) monocytes, we also compared the level of expression of CD16/FcγRIIIA according to the CD14 level and studied the relationship between CD16/FcγRIIIA expression and intracellular TNF-α production upon stimulation by ICs. CD16/FcγRIIIA expression was the highest overall on CD14+ CD16+ monocytes of children with SMA at enrollment. At convalescence, SMA children were the only ones to show a significant decline in the same parameter. In contrast, there were no significant differences among groups in the expression of CD16/FcγRIIIA on CD14++ CD16+ monocytes. A greater percentage of CD14+ CD16+ monocytes produced TNF-α upon stimulation than any other monocyte subset, and the amount of intracellular TNF-α correlated positively with CD16/FcγRIIIA expression. Furthermore, there was an inverse correlation between hemoglobin levels and CD16/FcγRIIIA expression in children with SMA and their controls. These data suggest that monocytes of children with SMA respond differently to Plasmodium falciparum infection by overexpressing CD16/FcγRIIIA as they mature, which could enhance erythrophagocytosis and TNF-α production.
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U2 - 10.1128/IAI.01078-09
DO - 10.1128/IAI.01078-09
M3 - Article
C2 - 20231419
AN - SCOPUS:77951217273
SN - 0019-9567
VL - 78
SP - 2173
EP - 2181
JO - Infection and Immunity
JF - Infection and Immunity
IS - 5
ER -