In a unique study area in Chile, our research group found that relative risks of adult mortality from cancer, bronchiectasis and tuberculosis (TB) are much greater when arsenic exposure occurred only in utero / early-life, rather than later in life. This provides rare human evidence in support of the “Developmental Origins of Health and Disease” (DOHaD) hypothesis. The focus here is on the effects of arsenic on macrophages, innate immune cells known to influence tumor progression and TB pathogenesis. Based on a combined metabolomics and multiplex cytokine/chemokine profiling approach, the results of this study provide a model for how early-life exposures may alter macrophage development and contribute to an overall immunomodulatory signaling landscape that drives delayed disease pathogenesis.
Speaker Biography - Fenna C.M. Sillé, Ph.D.
Fenna C.M. Sillé, Ph.D.
Environmental Health Sciences Division, School of Public Health, University of California, Berkeley
Dr. Fenna Sillé is a postdoctoral fellow in the Environmental Health Sciences division, School of Public Health at UC Berkeley. Her research goal is to understand how in utero and early-life exposures modulate the immune system and subsequently affect long-term disease risk. In 2004, she received her Master’s in immunology and molecular virology from the University of Groningen, The Netherlands. She received her PhD in immunology in 2010 from Utrecht University, The Netherlands, for her work as a Boehringer Ingelheim Fonds Fellow at the Brigham and Women’s Hospital and Harvard Institutes of Medicine. From 2011-2013, she performed her first postdoctoral research in functional immunogenomics at UC Berkeley. Her recent project focused on testing epigenetic changes as predictive biomarkers of exposure-related diseases. For her current research she combines immunotoxicology, functional genomics and metabolomics with exposure epidemiology to determine the effects of early-life arsenic exposure on macrophage function and tuberculosis risk.
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