CVI Accepts, published online ahead of print on 16 July 2008

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Clin. Vaccine Immunol. doi:10.1128/CVI.00506-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

LEVELS OF SOLUBLE CD163 AND MALARIA SEVERITY IN GHANAIAN CHILDREN

Kwadwo A. Kusi, Ben A. Gyan^*, Bamenla Q. Goka, Daniel Dodoo, George Obeng-Adjei, Marita Troye-Blomberg, Bartholomew D. Akanmori, and Jonathan P. Adjimani

Immunology Department, Noguchi Memorial Institute for Medical Research, College of Health Sciences, University of Ghana, Legon, Ghana; Department of Child Health, University of Ghana Medical School, College of Health Sciences, Korle-Bu Teaching Hospital, Accra, Ghana; Department of Immunology, Wenner-Gren Institute, Stockholm University, Stockholm, Sweden; Department of Biochemistry, University of Ghana, Legon, Ghana

^* To whom correspondence should be addressed. Email: bgyan{at}noguchi.mimcom.net.

CD163 is an acute phase-regulated monocyte/macrophage membrane receptor expressed late in inflammation. It is involved in the haptoglobin-mediated removal of free hemoglobin (Hb) from plasma and has been identified as a natural soluble plasma glycoprotein with potential anti-inflammatory properties, possibly linked to the individual's haptoglobin (Hp) phenotype. High levels of soluble CD163 (sCD163) in a malaria episode may therefore down-regulate inflammation and curb disease severity. In order to verify this, the relationships between sCD163 levels, malaria severity and selected inflammatory mediators (TNF-, IL6, IL10) were assessed by ELISA in plasma samples obtained from pediatric malaria patients with uncomplicated malaria (UM, N=38), cerebral malaria (CM, N=52) and severe malarial anemia (SA, N=55) during two consecutive malaria transmission seasons (2002 and 2003). Median sCD163 levels were higher in UM (11.9 µg/mL) than in SA (7.7 µg/mL, P = 0.010) and CM (8.0 µg/mL, P = 0.031). Levels of sCD163 were also higher in all patient groups as compared to a group of 81 age-matched healthy controls. The higher sCD163/TNF- ratio in UM, coupled with the fact that sCD163 levels correlated with TNF- levels in UM but not in CM and SA, suggests inflammatory dys-regulation in the complicated cases.

The study showed that sCD163 levels are elevated during acute malaria. High sCD163 levels in UM patients may be due to the induction of higher anti-inflammatory responses enabling them to avoid disease complications, or that UM patients simply lost their CD163 receptors from macrophages in inflammatory sites while complicated malaria groups still had their receptors attached to activated macrophages, reflecting on-going and higher inflammation associated with complicated malaria.