Research Assistant Professor Pharmaceutical Sciences Washington State University Pullman, WA 99164-6534   Phone: 509-335-8812 Fax: 509-335-5902 E-mail: vordersb@wsu.edu   Ph.D., 2000 - Toxicology, Oregon State University RESEARCH INTERESTS: Reproductive Toxicology (mammary gland and Immunotoxicology. RESEARCH SUMMARY: Our laboratory is interested in understanding the mechanisms of toxicity caused by activation of an orphan nuclear receptor known as the aryl hydrocarbon receptor (AhR). Numerous environmental pollutants activate the AhR, and we study the highest affinity ligand, TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, or “dioxin”). We have found that activation of the AhR during pregnancy impairs normal differentiation of the mammary gland, and are currently investigating a possible link between this impaired differentiation and breast cancer development. Another research interest is understanding how AhR activation alters the immune response to infectious disease. Currently we are examining the effects of TCDD on host resistance to Streptococcus pneumoniae infection.   REFEREED PUBLICATIONS Vorderstrasse, BA and BP Lawrence. (2006) Protection against lethal challenge with Streptococcus pneumoniae is conferred by activation of the aryl hydrocarbon receptor, but is not associated with an enhanced inflammatory response. Infection and Immunity. 74(10): 5679-86. Vorderstrasse, BA, JA Cundiff, and BP Lawrence. (2006) A dose-response study of the effects of prenatal and lactational exposure to TCDD on the immune response to influenza A virus. Journal of Toxicology and Environmental Health, pt. A. 69(6):445-63. Vorderstrasse, BA, JA Cundiff, and BP Lawrence. (2004) Developmental exposure to the potent aryl hydrocarbon receptor agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin impaires the cell-mediated immune response to infection with influenza A virus, but enhances elements of innate immunity. J. Immunotox. 1:103-112. Lawrence, BP, and BA VORDERSTRASSE. (2004) Activation of the aryl hydrocarbon receptor diminishes the memory response to homotypic influenza virus infection but does not impair host resistance. Toxicol. Sci. 79: 304-314. VORDERSTRASSE, BA, SE Fenton, AA Bohn, JA Cundiff, and BP Lawrence. (2004) A novel effect of dioxin: Exposure during pregnancy severely impairs mammary gland differentiation. Toxicol. Sci. 78:248-257. Neff-LaFord, HD, BA VORDERSTRASSE, and BP Lawrence. (2003) Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice. Cellular Immunology 226:54-64. VORDERSTRASSE, B.A., A.A. Bohn, and B.P. Lawrence. (2003) Examining the relationship between impaired host resistance and altered immune function in mice treated with TCDD. Toxicology. 188:15-28. Vorderstrasse, BA, E.D. Dearstyne, and N.I Kerkvliet. (2003) Influence of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the antigen-presenting activity of dendritic cells. Toxicol. Sci. 72:103-112. VORDERSTRASSE, B.A., and N.I. Kerkvliet. (2001) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) affects the number and function of murine splenic dendritic cells and their expression of accessory molecules. Toxicol. Appl. Pharmacol. 171:117-125. Vorderstrasse, B.A., Steppan, L.B., Silverstone, A.E., and N.I. Kerkvliet. (2001) Aryl hydrocarbon receptor-deficient mice generate normal immune responses to model antigens and are resistant to TCDD-induced immune suppression. Toxicol. Appl. Pharmacol. 171:157-164. Kerkvliet, N.I., Baecher-Steppan, L., Shepherd, D.M., Oughton, J.A., Vorderstrasse, B.A., and G.K. DeKrey. (1996) Inhibition of TC-1 cytokine production, effector cytotoxic T lymphocyte development and alloantibody production by 2,3,7,8-tetrachlorodibenzo-p-dioxin. J. Immunol. 157:2310-2319. Jagielo, T.H., LeClair, L.L., and B.A. Vorderstrasse. (1996) Genetic variation and population structure of lingcod. Transactions of the American Fisheries Society. 125:372-386.