Dr. Bullard’s research interests are centered on defining the mechanisms that regulate inflammation. For these investigations, we have focused our studies on defining the roles of leukocyte/endothelial cell adhesion molecules in mediating inflammatory responses. These proteins, along with chemoattractant/activating molecules, mediate the process by which leukocytes exit the vasculature into tissue in response to an inflammatory stimulus. Many different adhesion molecules have been described, including the selectins, integrins, and members of the immunoglobulin superfamily of adhesion receptors. Recent evidence from our lab and others suggest that these molecules play both pro- and anti-inflammatory roles, and we are using a genetic approach in mice to further define these functions. For our studies, we have developed many different lines of adhesion molecule mutant mice using gene-targeting methodologies. Mice with single or multiple mutations are currently being analyzed in models of rheumatoid arthritis, lupus erythematosus, vasculitis, and inflammatory bowel disease to determine their specific roles in the pathogenesis of these diseases. Our lab has also characterized a novel model for psoriasis and psoriatic arthritis that develops in Beta-2 integrin mutant mice backcrossed onto the PL/J strain background. We are now trying to map and clone the genes that control the development of both the skin disease and the arthritis in this model system.
