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Martha FurieResearch InterestsIn areas of inflammation, leukocytes (white blood cells) leave the bloodstream and enter the surrounding tissues, where they can then carry out their functions in host defense. However, if the leukocytes accumulate inappropriately or excessively, the potent anti-microbial substances that they secrete may contribute to tissue damage and worsen disease. To exit from the bloodstream, a circulating leukocyte must first adhere to and then migrate across the layer of endothelial cells that lines the blood vessel wall. A major focus of our research is to identify the molecular mechanisms that control the movement of leukocytes across the vessel wall, particularly in the context of bacterial infections. Our efforts center on two bacterial illnesses. The first is Lyme disease, which is a chronic inflammatory condition caused by the bacterium B. burgdorferi. The second is tularemia, an often-fatal illness caused by Francisella tularensis. Due to its high infectivity and exceptional virulence, F. tularensis is classified as a potential bioweapon. For both of these bacteria, we are using in vitro and in vivo approaches to understand how the inflammatory response of the infected host contributes to development of disease. Much of our research is performed with cultured primary human endothelial cells and leukocytes, but we also make use of mouse models of Lyme disease and tularemia. Our results and those of other research groups suggest that B. burgdorferi incites an excessive yet ineffective inflammatory response, leading to arthritis, carditis, and neurological symptoms in affected individuals. |
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