Host cell-pathogen interactions between erythrocytes and P. falciparum: apoptotic mimicry?

Abstract

Understanding the phagocytic process of malaria-infected erythrocytes and the subsequent cascade of host response are important in developing new strategies for treating malaria. In this study, we focused on phosphatidylserine (PS) and its possible role in malaria pathogenesis through phagocytosis. Plasmodium falciparum was found to induce PS exposure in both infected and uninfected erythrocytes which could represent a form of apoptotic mimicry; therefore, aiding in parasite perpetuation and immune evasion. A new phagocytic assay was developed, using dihydroethidine and CellTraceTM Violet. While both infected and uninfected erythrocytes in P. falciparum cultures were phagocytosed by THP-1 cells, addition of Annexin V did not inhibit phagocytosis. However, an increase in IL-6 production and a decrease in IL-10 production were observed, suggesting upregulation of pro-inflammatory signals through the blocking of PS. In conclusion, the role of PS still remains unclear; however, the presence of apoptotic mimicry in P. falciparum cannot be ruled out.