Distinct brain and lung endothelial miRNA/mRNA profiles after exposure to Plasmodium falciparum-infected red blood cells.

MicroRNAs (miRNAs) control 60% of genes expressed in the human body, but their role in malaria pathogenesis is incompletely understood. Here, we demonstrate cell type-specific alterations to the miRNA profiles during the early response to malaria infection in brain and lung endothelial cells (ECs). In brain ECs, incubation with Plasmodium falciparum-infected red blood cells in the ring stage (iRBCs) most significantly affected endocytosis-related miRNAs and mRNAs. Contrastingly, in lung ECs, iRBCs altered electron transport chain-related miRNAs and mRNAs. We present a dataset of inherent differences between microRNA profiles in brain and lung ECs and their extracellular vesicles (EVs). We demonstrated that shear stress affected multiple pathways in brain ECs, which were controlled by numerous human miRNAs. Together, these findings indicate that host miRNAs respond to parasite exposure, accompanied by stimulation of downstream signaling pathways within the ECs. Therefore, we consider miRNAs the initial spark for early host-parasite interaction events.