Martha Furie

Research Interests

In areas of inflammation, 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 white blood cells 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 white blood cell 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 white blood cells across the vessel wall, particularly in the context of infectious diseases. Much of our effort in the past few years has focused on Lyme disease, a chronic inflammatory condition that is caused by the bacterium Borrelia burgdorferi. Using tissue culture models of the vessel wall, we have shown that B. burgdorferi causes endothelial cells to express adhesion molecules that bind to white blood cells and to secrete soluble factors that attract the white cells. As a consequence, various types of white blood cells adhere to and migrate across monolayers of endothelial cells that have been exposed to B. burgdorferi. At present, we are examining in detail the ability of B. burgdorferi to stimulate the transendothelial migration of a particular type of white blood cell called the type 1 T lymphocyte. Type 1 T cells secrete factors that perpetuate and amplify an inflammatory response, and they appear to be particularly abundant in the lesions of patients with Lyme disease. In addition, we are studying the mechanisms whereby interleukin-10, a naturally occurring host factor, prevents stimulation of endothelial cells by B. burgdorferi and other bacterial agents.