Innate Immune–Bacterial Interactions During Chronic Bacterial Infection

The oral cavity is a unique environment is which many bacteria present in the dental plaque are in constant close contact with the host resident and immune cells. We are interested in studying how oral spirochetes such as Treponema denticola that are associated with periodontal disease, manipulate the innate immune response to allow bacterial survival and progressive disease. The major outer sheath protein (Msp) of T. denticola is a prominent virulence factor produced by this organism, which is able to impair the normally protective neutrophil immune response through inhibition of directed cell migration (chemotaxis). This inhibition occurs through inappropriate modulation of lipid signaling phosphoinositide metabolism and related actin rearrangement pathways. We use a variety of tools and techniques to investigate these lipid signaling processes and other initial events occurring in host cells leading to modulation of the appropriate immune response.

A second area of research in my laboratory involves investigating less well understood cytokines and inflammatory mediators produced by immune cells in response to oral bacteria during periodontal disease. We are also examining the role of these cytokines in modifying the function of host tissue resident cells such as gingival epithelial and fibroblast cells.