EVIDENCE OF ENDOTHELIAL INFLAMMATION, T-CELL ACTIVATION, AND T-CELL REALLOCATION IN UNCOMPLICATED PLASMODIUM-FALCIPARUM MALARIA

To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to re spond to antigenic stimulation in vitro, we have postulated the diseas e-induced reallocation of peripheral lymphocytes, possibly by adhesion to inflamed endothelium. We measured plasma levels of soluble markers of endothelial inflammation and T cell activation in 32 patients suff ering from acute, uncomplicated P. falciparum malaria. as well as in 1 0 healthy, aparasitemic control donors. All donors were residents of a malaria-endemic area of Eastern State Sudan. In addition, we measured the T cell surface expression of the interleukin-2 receptor (CD25) an d the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We f ound that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with th e control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in th e CD4(+) subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.