摘要：SummaryTrypanosoma bruceiis the causative agent of human African trypanosomiasis. The parasite transmigrates from blood vessels across the choroid plexus epithelium to enter the central nervous system, a process that leads to the manifestation of second stage sleeping sickness. Using anin vitromodel of the blood-cerebrospinal fluid barrier, we investigated the mechanism of the transmigration process. For this, a monolayer of human choroid plexus papilloma cells was cultivated on a permeable membrane that mimics the basal lamina underlying the choroid plexus epithelial cells. Plexus cells polarize and interconnect forming tight junctions. Deploying differentT. brucei bruceistrains, we observed that geometry and motility are important for tissue invasion. Using fluorescent microscopy, the parasite’s moving was visualized between plexus epithelial cells. The presented model provides a simple tool to screen trypanosome libraries for their ability to infect cerebrospinal fluid or to test the impact of chemical substances on transmigration.Graphical abstractDisplay OmittedHighlights•HIBCPP cells on Transwell filters were used as a model of the blood-CSF barrier•Transmigration efficiency ofTrypanosoma brucei bruceiwas quantified by qPCR•Transmigration seemed independent of major surface metalloprotease B•Transmigration might be a mechanical process affected by parasite geometry/motilityMicrobiology; Parasitology; Bioengineering
