Plasmodium falciparum isolates from patients with uncomplicated malaria promote endothelial inflammation.

The ability of Plasmodium falciparum infected erythrocytes (Pf-IEs) to activate endothelial cells has been described; however, the interaction of the endothelium with Pf-IEs field isolates from patients has been less characterized. Previous reports have shown that isolates alter the endothelial permeability and apoptosis. In this study, the adhesion of 19 uncomplicated malaria isolates to Human Dermal Microvascular Endothelial Cells (HDMEC), and their effect on the expression of ICAM-1 and proinflammatory molecules (sICAM-1, IL-6, IL-8, and MCP-1) was evaluated. P. falciparum isolates adhered to resting and TNFα-activated HDEMC cells at different levels. All isolates increased the ICAM-1 expression on the membrane (mICAM-1) of HDMEC and increased the release of its soluble form (sICAM-1), as well the production of IL-6, IL-8 and MCP-1 by HDMEC with no signs of cell apoptosis. No correlation between parasite adhesion and production of cytokines was observed. In conclusion, isolates from uncomplicated malaria can induce a proinflammatory response in endothelial cells that may play a role during the initial inflammatory response to parasite infection; however, a continuous activation of the endothelium can contribute to pathogenesis.