Tuesday, April 16, 2024
4/16/2024
Project Summary/Abstract: Neurobrucellosis is the most morbid complication of Brucella infection in humans, but studies on neurobrucellosis are scarce due to the lack of relevant animal models. In this proposal, we present the first murine models of neurobrucellosis in which Brucella is able to colonize the brain, induce inflammation, and impair neurologic function. We found marked upregulation of transcriptional signatures associated with interferon (IFN) signaling and complement activation in the brains of mice with neurobrucellosis. In addition, we found that IFNs restrict neurologic complications of brucellosis. In Specific Aim #1 of this proposal, we will investigate the cell types and signaling pathways responsible for IFN-mediated protection against neurobrucellosis. In Specific Aim #2, we will investigate whether interactions between complement and IFNs are involved in the pathogenesis of neurobrucellosis. Collectively, our results will enhance our basic understanding of neurobrucellosis, and potentially identify targets for complementary therapeutics for neurobrucellosis.
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