“My research investigates the interaction between Plasmodium falciparum infected red blood cells and the vascular endothelium, and how these interactions lead to mild versus severe malaria. My focus is on parasite adhesion proteins (PfEMP1) and how they bind to specific endothelial receptors under physiologically relevant blood-flow conditions. Using genetically defined parasite lines, organ specific endothelial cells, flow-based adhesion assays and transcriptomics, I analyse how different binding modes (rolling versus static) activate endothelial cells. My aim is to identify receptor–ligand interactions that trigger pathogenic endothelial responses, and to establish whether preventing static adhesion alone is sufficient to prevent severe malaria.”

"My project aims at investigating the intestinal invasion of Entamoeba histolytica. I try to decipher the role of cysteine peptidases of Entamoeba histolytica in tissue breakdown. I focus on a Caco-2 cell model currently. Furthermore, I am establishing patient-derived colon organoids and induced-pluripotent stem cell derived colon organoids. Data of the Caco-2 model and organoid models will be assessed in terms of cost-effectiveness, reliability and data quality."

“In my project, I focus on the interaction between the human malaria parasite Plasmodium falciparum and the human vascular endothelium. Infected red blood cells adhere to endothelial cell receptors, leading to impaired blood flow, inflammation, and endothelial dysfunction. This process is mediated by PfEMP1 proteins displayed on the surface of infected cells. I investigate how differences in endothelial cell origin and physiological conditions such as shear stress and temperature influence endothelial responses to cytoadhesion. Ultimately, this research seeks to improve our understanding of host-parasite interactions underlying severe malaria.”