My research focuses on the molecular mechanisms of intracellular trafficking with particular emphasis on the ability of pathogens to alter normal cellular trafficking events to evade clearance by the host.
Legionella pneumophila, the causative agent of Legionnaire’s disease, is a gram-negative bacterium that lives in fresh water amoeba and which can also invade human macrophages in the lung. L. pneumophila inhibits normal intracellular transport to lysosomes where the bacteria would be destroyed and then recruits host cell ER-derived vesicles to its vacuolar membrane. Both of these processes are dependent on the expression of a functional type IV secretion apparatus called the Dot/Icm system. This apparatus allows Legionella to inject bacterial effector proteins in the host cell cytosol. Remodeling of the L. pneumophila-containing vacuole creates an intracellular environment permissive for bacterial growth.
My laboratory is currently working on identifying the L. pneumophila proteins responsible for the recruitment and fusion of host cell vesicles to the vacuolar membrane.