Interferons in Neurobrucellosis

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.

Grant Number: 5R21AI178158-02
NIH Institute/Center: NIH
Principal Investigator: Mostafa Ateya Abushahba