The effect of Plasmodium falciparum infection on expression of monocyte surface molecules

• Published in: Transactions of the Royal Society of Tropical Medicine and Hygiene Vol. 100; no. 11; pp. 1007 - 1012
• Main Authors: Jenkins, N.E., Chakravorty, S.J., Urban, B.C., Kai, O.K., Marsh, K., Craig, A.G.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01-11-2006; Royal Society of Tropical Medicine and Hygiene; Elsevier
• Subjects: Biological and medical sciences; CCR5; CD23; CD87; Child; Child, Preschool; Flow Cytometry; Human protozoal diseases; Humans; ICAM-1; Infant; Infant, Newborn; Infectious diseases; Malaria; Malaria, Falciparum - metabolism; Malaria, Falciparum - parasitology; Medical sciences; Membrane Proteins - metabolism; Monocytes; Monocytes - metabolism; Monocytes - parasitology; Parasitic diseases; Phenotype; Plasmodium falciparum; Protozoal diseases; uPAR; Plasmodium falciparum; Monocytes; Malaria; ICAM-1; uPAR; CCR5; CD23; CD87; Protozoal disease; u-Plasminogen activator; Tropical medicine; Child; Biological receptor; Human; Protozoa; Apicomplexa; Serine endopeptidases; Monocyte; Pathophysiology; Intercellular adhesion molecule 1; Enzyme; Parasitosis; Infection; CCR5 chemokine receptor; Peptidases; Hydrolases
• ISSN: 0035-9203; 1878-3503
• DOI: 10.1016/j.trstmh.2006.01.005

Plasmodium falciparum infection may result in severe malaria in susceptible individuals. The pathogenesis of severe disease is probably a combination of the sequestration of infected erythrocytes and overstimulation of the immune response. Monocytes are a key source of many of the pro-inflammatory agents implicated but also are found sequestered in blood vessels. However, little is known about the monocyte phenotype in malaria disease. Flow cytometry was performed on fresh whole blood to determine surface expression of four receptors during acute severe and non-severe malaria and again during convalescence when uninfected. Three hundred and fifty-six children with
P. falciparum infection were studied and were found to show increased expression of intercellular adhesion molecule-1 (ICAM-1), urokinase plasminogen activator receptor (uPAR), CD23 and chemokine receptor 5 (CCR5) (
P
<
0.001) during acute disease compared with convalescent levels. Using multivariate analysis, it was found that large increases in expression of ICAM-1 (odds ratio (OR) 2.44, 95% CI 1.80–3.32) and uPAR (OR 3.14, 95% CI 1.93–5.09) but small increases in expression of CD23 (OR 0.82, 95% CI 0.68–0.96) were independently associated with severe malaria. These results give an insight into the cellular processes occurring in severe malaria and suggest that pathology is based on a complex repertoire of pro- and anti-inflammatory processes.