Beschreibung:
<jats:title>ABSTRACT</jats:title><jats:p><jats:bold>Objective</jats:bold>: <jats:italic>Plasmodium falciparum</jats:italic> malaria in humans and animal models of this disease have revealed changes in the infected host that are consistent with a systemic inflammatory response. Although it has been proposed that endothelial cell adhesion molecules (CAM) contribute to the adhesive interactions of <jats:italic>Plasmodium</jats:italic>‐infected erythrocytes and immune cells with vascular endothelial cells, ECAM expression has not been systematically studied in <jats:italic>Plasmodium</jats:italic>‐infected animals.</jats:p><jats:p><jats:bold>Methods</jats:bold>: In this study, the dual radiolabeled monoclonal antibody method was used to quantify the expression of different ECAMs (ICAM‐1, VCAM‐1, P‐selectin, E‐selectin) in different regional vascular beds of <jats:italic>Plasmodium berghei</jats:italic> ANKA‐inffected mice (<jats:italic>PbA</jats:italic>), a well‐recognized model of human cerebral malaria. The roles of T lymphocytes and certain cytokines (TNF‐α, IL‐12, IFN‐γ) in mediating the infection‐induced expression of ICAM‐1 and P‐selectin were assessed by using relevant mutant mice.</jats:p><jats:p><jats:bold>Results</jats:bold>: Wild‐type (WT) mice exhibited highly significant increases in the expression of ICAM‐1, VCAM‐1, and P‐selectin (but not E‐selectin) in all vascular beds on the 6th day of <jats:italic>PbA</jats:italic> infection. The <jats:italic>PbA</jats:italic>‐induced upregulation of ICAM‐1 was significantly blunted in mice that were either deficient in IFN‐α, IL‐12 (but not TNF1b) or T lymphocytes (Rag‐1 deficiency); however, these responses were tissue specific.</jats:p><jats:p><jats:bold>Conclusions</jats:bold>: These findings indicate that vascular endothelial cells in most regional circulations assume an inflammatory phenotype and that cytokines and immune cells mediate this response in a tissue‐specific manner.</jats:p>