A murine model of Lyme disease demonstrates that Borrelia burgdorferi colonizes the dura mater and induces inflammation in the central nervous system

Lyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, nervous systems including central system (CNS). Inbred laboratory mice have been used define kinetics of B . host immune responses in joints however similar studies are lacking CNS these animals. A tractable animal model for investigating host- interactions key understanding mechanisms pathogenesis. Therefore, we characterized colonization associated during early subacute infection. Using fluorescence-immunohistochemistry, intravital microscopy, bacterial culture, quantitative PCR, found routinely colonized dura mater C3H mice, peak spirochete burden at day 7 post-infection. Dura was observed several disease agents , garinii mayonii RNA-sequencing RT-PCR showed that increased expression cytokines a robust interferon (IFN) response mater. Histopathologic changes leukocytic infiltrates vascular were also meninges infected In contrast meninges, did not detect infiltrating leukocytes, or large-scale cytokine profiles cerebral cortex hippocampus infection; however, both brain regions demonstrated IFN-stimulated genes as peripheral tissues meninges. Taken together, capable colonizing induces localized inflammation tissues. sterile IFN absence unique parenchyma, provides insight into potential pathology this important pathogen.