Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria

TY - JOUR

T1 - Evidence of endothelial inflammation, T cell activation, and T cell reallocation in uncomplicated Plasmodium falciparum malaria

AU - Elhassan, I M

AU - Hviid, L

AU - Satti, G

AU - Akerstrom, B

AU - Jakobsen, P H

AU - Jensen, J B

AU - Theander, T G

N1 - Keywords: Adolescent; Adult; Animals; Cell Adhesion; Cell Adhesion Molecules; Confidence Intervals; Cross-Sectional Studies; E-Selectin; Endothelium, Vascular; Female; Humans; Immunophenotyping; Inflammation; Intercellular Adhesion Molecule-1; Lymphocyte Activation; Lymphocyte Function-Associated Antigen-1; Malaria, Falciparum; Male; Middle Aged; T-Lymphocytes; Vascular Cell Adhesion Molecule-1

PY - 1994

Y1 - 1994

N2 - To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-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 suffering from acute, uncomplication P. falciparum malaria, as well as in 10 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) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.

AB - To explain the observation that acute Plasmodium falciparum malaria is associated with a transient inability of peripheral blood cells to respond to antigenic stimulation in vitro, we have postulated the disease-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 suffering from acute, uncomplication P. falciparum malaria, as well as in 10 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) and the lymphocyte function-associated antigen (LFA-1; CD11a/CD18). We found that the plasma levels of all inflammation and activation markers were significantly increased in the malaria patients compared with the control donors. In addition, we found a disease-induced depletion of T cells with high expression of the LFA-1 antigen, particularly in the CD4+ subset. The results obtained provide further support for the hypothesis of T cell reallocation to inflamed endothelium in acute P. falciparum malaria.

M3 - Journal article

C2 - 7524374

SN - 0002-9637

VL - 51

SP - 372

EP - 379

JO - Journal. National Malaria Society

JF - Journal. National Malaria Society

IS - 3

ER -