<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Speidel A</submitter><funding>Eberhard Karls Universität Tübingen</funding><pagination>104014</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8933718</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>25(4)</volume><pubmed_abstract>&lt;i>Trypanosoma brucei&lt;/i> is 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 an &lt;i>in vitro&lt;/i> model 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 different &lt;i>T. brucei brucei&lt;/i> strains, 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.</pubmed_abstract><journal>iScience</journal><pubmed_title>Transmigration of &lt;i>Trypanosoma brucei&lt;/i> across an &lt;i>in vitro&lt;/i> blood-cerebrospinal fluid barrier.</pubmed_title><pmcid>PMC8933718</pmcid><funding_grant_id>2465-0-0</funding_grant_id><pubmed_authors>Theile M</pubmed_authors><pubmed_authors>Duszenko M</pubmed_authors><pubmed_authors>Schwerk C</pubmed_authors><pubmed_authors>Schroten H</pubmed_authors><pubmed_authors>Pfeiffer L</pubmed_authors><pubmed_authors>Mogk S</pubmed_authors><pubmed_authors>Figarella K</pubmed_authors><pubmed_authors>Herrmann A</pubmed_authors><pubmed_authors>Speidel A</pubmed_authors><pubmed_authors>Ishikawa H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transmigration of &lt;i>Trypanosoma brucei&lt;/i> across an &lt;i>in vitro&lt;/i> blood-cerebrospinal fluid barrier.</name><description>&lt;i>Trypanosoma brucei&lt;/i> is 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 an &lt;i>in vitro&lt;/i> model 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 different &lt;i>T. brucei brucei&lt;/i> strains, 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.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-18T20:23:31.967Z</modification><creation>2025-04-07T08:19:22.807Z</creation></dates><accession>S-EPMC8933718</accession><cross_references><pubmed>35313698</pubmed><doi>10.1016/j.isci.2022.104014</doi></cross_references></HashMap>