Adjunct Professor of Microbiology
Professor and Chair of Periodontics
Office Location: Health Sciences D-674, D-652
Campus Box: 357444
Dr. Darveau received his Ph.D. in bacteriology from Washington State University and did his postdoctoral research in the Department of Microbiology at the University of British Columbia studying structure/function relationships in the outer membrane of Pseudomonas aeruginosa. He is a Research Professor in the Department of Periodontics.
Our research is centered on the innate host response to microbial colonization and infection. We are keenly interested in the inflammatory component of the innate host response. Our laboratory studies both the microbial components that elicit inflammation and the activation pathways employed by the host in response to different microbial components. We study responses to both commensal and pathogenic bacteria. We employ biochemical isolation and analytical techniques to characterize the microbial components. Examples of microbial components that we have studied are lipopolysaccharide form gram negative bacteria and lipoteichoic acid from gram positive bacteria. We use a variety of different in vitro cell culture systems to analyze host responses. Examples of systems that have used are human and mouse endothelial cells, human epithelial cells, human and mouse monocytes. We also construct cell lines (both stable and transient) to examine select components of the host innate response system.
The goal of our laboratory is to understand how the host discriminates between commensal and pathogenic bacteria and in turn how bacteria may capitalize on these host pathways to create disease.
Roberts, F.A. and R. P. Darveau. 2002. Beneficial Bacteria of the Periodontium Periodontology 2000 30: 40-50.
Darveau, R. P. 2000. Oral innate host defense responses: interactions with microbial communities and their role in the development of disease. pp 170-202 In "Oral Bacterial Ecology: The Molecular Basis", Howard K. Kuramitsu and Richard Ellen, eds.
Cunningham, M.D, Shapiro, R.A., Seachord, C., Ratcliffe, K., Cassiano, L., and Darveau, R.P. 2000. CD14 employs hydrophilic regions to "capture" Lipopolysaccharide. J. Immunology 164: 3255-63.
Darveau, R. P., Arbabi, S, Garcia, I., Bainbridge, B., and Maier, R.V. 2002. Porphyromonas lipopolysaccharide is both an agonist and antagonist for p38 MAP kinase activation. Infection & Immunity 70: 1867-1873.