Research in my lab is focused in areas of host-pathogen interaction geared toward developing a better understanding of the host mechanisms and bacterial structures important in infection-elicited inflammation. To accomplish this we use a variety of approaches including molecular, cellular, immunological, and animal modeling to develop a synthetic understanding of relevant systems. Work has centered on identification of host cell receptors engaged by key bacterial structures/adhesins, and the subsequent signaling pathways activated which lead to immune activation, with the goal to harness those factors in a manner that can lead to re-establishment of normal tissue homeostasis. Current investigative lines utilize the bacterium Porphyromonas gingivalis as a model oral organism to study key facets of anaerobic bacterial infection and contribution of bacterial structures such as capsular polysaccharides in the development of inflammation and oral bone loss. A particular area of interest is identification of molecular targets and pathways that could serve as novel points for therapeutic intervention to augment available treatments aimed to limit periodontal tissue destruction.
In addition to the work focusing on the pathogenesis of oral disease, our group engaged in collaborative studies that have been seminal in identifying associations of oral bacterial infection with cardiovascular disease. Work in this area provides experimental evidence that P. gingivalis is a potential risk factor for atherosclerosis, and that this infection-elicited acceleration can be prevented through immunization. The underlying mechanisms of this association are not well defined. More recently we have become interested in nuclear hormone receptors including liver x receptors and peroxisome proliferator-activated receptors in the development of bacteria-elicited inflammation, and contribution of inflammatory cues at sites of infection in the pathogenesis of periodontal disease. Furthermore, collaborative studies have begun to explore P. gingivalis interactions with adipocytes, as well as integrative studies to investigate aspects of P. gingivalis / HIV co-infection.
- Bacterial pathogenesis
- Host-pathogen interaction
- Infection and systemic disease