Martha Furie

Research Interests (continued)

Currently, we are dissecting the role of the host cytokine interferon-gamma (IFN) in the pathogenesis of Lyme disease. Our data indicate that B. burgdorferi and IFN act in concert to promote changes in endothelial cells that favor the accumulation of long-lived, chronic inflammatory leukocytes in infected lesions. At the same time, these agents work together to suppress the recruitment of short-lived inflammatory cells that typify acute inflammation. IFN may thus act as a molecular “switch” that controls the transition from acute to chronic inflammation.
Whereas B. burgdorferi elicits an exaggerated inflammatory response, F. tularensis stimulates endothelial cells and leukocytes very poorly. Moreover, F. tularensis invades and replicates in macrophages, which normally serve to destroy microorganisms. The ability of F. tularensis to elude normal host-defense mechanisms undoubtedly contributes to its high infectivity and virulence. At present, we are focused on understanding how F. tularensis actively suppresses stimulation of endothelial cells, thereby preventing recruitment of leukocytes to areas of infection. We are also studying the interactions of F. tularensis with hepatocytes, the major cells of the liver. Like macrophages, hepatocytes support the intracellular growth of F. tularensis to high numbers, but the mechanisms that the bacterium uses to adapt to this intracellular niche are not well-understood. 

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