The Lyme disease bacterium, Borrelia burgdorferi, stimulates an inflammatory response in human choroid plexus epithelial cells
We report the results of gene expression profiling via RNA-sequencing of primary human choroid plexus epithelial cells in vitro that were infected with Borrelia burgdorferi, the causative agent of Lyme disease. Epithelial cells were cultured with B. burgdorferi for 48 hours prior to RNA isolation. Following high-throughput sequencing via Illumina HiSeq 4000, a total of 258 differentially expressed genes were identified. Subsequent data analysis indicates an inflammatory and immune response generated by the epithelial cells following infection, marked by chemotactic cytokines and interferon stimulated genes. Several genes associated with tight and adherens junctions were found to be downregulated. These data represent the first study to investigate the impact of B. burgdorferi on choroid plexus epithelial cells, implicating the choroid plexus in the pathogenesis of neurological manifestations of Lyme disease. Overall design: Primary human choroid plexus epithelial cells were infected with B. burgdorferi in vitro for 48 hours. RNA was isolated and sequenced via Illumina HiSeq 4000