Bio: I completed PhD degrees in Environmental Science and Neural Science at Indiana University in Bloomington, Indiana, US. I obtained postdoctoral training in ecotoxicology and environmental toxicology at Indiana University and additional postdoctoral training in immunotoxicology at the US Environmental Protection Agency in Research Triangle Park, North Carolina. I then moved into a tenure-track Assistant Professor position in the Department of Pharmacology and Toxicology of the Brody School of Medicine at East Carolina University in 2008. I moved to the rank of tenured Associate Professor in 2015 and then to Professor in 2022. In 2023 I transferred my laboratory to the Department of Environmental and Molecular Toxicology at Oregon State University where I am a Professor and also Director of the Pacific Northwest Center for Translational Environmental Health Research. My current work is informed by my training in environmental science, neurotoxicology, and immunotoxicology and my laboratory’s focus is on how emerging environmental contaminants affect the immune system and the interplay between the immune and nervous systems. 

Abstract: Per- and polyfluoroalkyl substances (PFAS), synthetic organic chemicals used in an array of products and processes, are contaminants of global concern that have been banned, phased out, restricted, and regulated due to their known and putative human and environmental health effects. Despite accumulated evidence of their toxicological hazards and health risks, the molecular mechanisms by which they induce toxicity are still active areas of research inquiry. Suppression of the vaccine antibody response is an adverse outcome that has been observed in exposed experimental models and humans, but a clear picture of the underlying molecular dysfunction has not been elucidated. Our laboratory hypothesizes B cell metabolism is perturbed by PFAS exposure, leading to deficiencies in B cells to respond appropriately to the metabolic challenges of activation, proliferation, and differentiation. Our findings with B cells isolated from mice exposed to PFAS in vivo indicate that exposed B cells become hypermetabolic upon activation, have insufficient mitochondrial reserve capacity, and thus fail to differentiate and proliferate, leading to shifts in B cell subsets and subsequent decreases in antibody levels. This talk will focus on our ongoing work with B cell immunometabolism and how PFAS exposure suppresses the vaccine antibody response through mitochondrial dysfunction.