Studies on the mechanism by which malaria parasites invade erythrocytes using host erythrocyte-derived ATP

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It was demonstrated that: i) ATP was released from infected erythrocytes upon burst. ii) ATP-stimulation resulted in phosphorylation of dematin, leading to loosening of membrane skeleton. iii) P2Y11 receptor antagonists inhibited malaria parasite invasion of erythrocytes. iv) The parasite invasion was inhibited in the presence of ATP-hydrolyzing enzymes. Altogether, it was strongly implicated that invasion process of erythrocytes by Plasmodium falciparum requires host erythrocyte-derived ATP, which then stimulates P2Y11-mediated signaling pathway, leading to phosphorylation of dematin, and loosening of erythroycte membrane skeleton. Drugs which shut down the above-mentioned signaling pathway might provide a novel strategy to protect humans from malaria.