SOLUBLE INTERCELLULAR-ADHESION MOLECULE-1 (ICAM-1), ENDOTHELIAL-LEUKOCYTE ADHESION MOLECULE-1 (ELAM-1), AND TUMOR-NECROSIS-FACTOR RECEPTOR (55 KDA TNF-R) IN PATIENTS WITH ACUTE PLASMODIUM-FALCIPARUM MALARIA

Adhesion of Plasmodium falciparum-infected erythrocytes to vascular en dothelium is in part mediated by ICAM-1 and ELAM-1 (E-selectin), which can be induced via the 55-kDa TNF-receptor (TNF-R55kDa). We have stud ied serum levels of soluble ICAM-1 (sICAM-1), ELAM-1 (sELAM-1), and so luble TNF-R55kDa (sTNF-R55kDa) in 37 patients with uncomplicated P. fa lciparum infection and in 17 control subjects in Bangkok, Thailand. Th e serum levels of sICAM-1 were markedly elevated in patients prior to treatment (601 +/- 239 ng/ml versus 160 +/- 47 ng/ml in healthy contro ls). In addition, elevated levels of sELAM-1 (53.6 +/- 23.1 ng/ml vers us 21.5 +/- 10.1 ng/ml) and sTNF-R55kDa (4.7 +/- 3.2 ng/ml versus 1.0 +/- 0.4 ng/ml) were observed (P < 0.05 for all). Soluble ELAM-1 reache d normal levels on Day 3, and sTNF-R55kDa on Day 14, while sICAM-1 was still significantly elevated 28 days after treatment was started (P < 0.05 for all). A correlation between sTNF-R55kDa (P < 0.05) and sELAM -1 (P < 0.05), respectively, with parasitemia prior to antimalarial tr eatment was found. These results suggest that a TNF-mediated expressio n of adhesion molecules induced by the asexual stage of malaria parasi tes serves as an immune-evasion mechanism. (C) 1994 Academic Press, In c.