Sílvia Sanz

The paper investigates how innate immune responses to Plasmodium falciparum contribute to blood-brain barrier disruption in cerebral malaria using an in vitro model.

The paper shows that fever increases adhesion of malaria parasites and neutrophils to brain blood vessels by damaging the endothelial glycocalyx, suggesting antipyretics could reduce disease severity.

This study shows that Plasmodium falciparum egress products disrupt BBB endothelial junctions and activate JAK-STAT signaling, leading to increased permeability and suggesting therapeutic targets.