Charles Parkos, MD, PhD is the Carl V. Weller Professor and Chair of the Department of Pathology at the University of Michigan Medical School. He received his MD/PhD degree from the University of California at San Diego and Scripps Research Institute in 1987, where his studies centered on determining the molecular basis of reactive oxygen species generation by neutrophils and identification of the molecular defect in Chronic Granulomatous Disease. In 1988, Dr. Parkos began residency and fellowship training in Pathology at Brigham and Women’s Hospital, with subspecialization in diagnostic gastrointestinal surgical pathology. While at Harvard Medical School, he began investigating fundamental mechanisms of dysregulated leukocyte trafficking across the intestinal mucosa, as observed in people with Inflammatory Bowel Disease (IBD). Dr. Parkos received his first independent NIH grant in 1995 and has been continuously R01-funded by multiple grants for over 25 years. In 1997, he was recruited to Emory University School of Medicine as a senior faculty member and Director of the Division of Gastrointestinal Pathology, and became a full Professor in 2003. In 2008 he was appointed Vice Chair in the Department of Pathology and Laboratory Medicine and Director of Experimental Pathology at Emory University School of Medicine. In September 2014 he was recruited to the University of Michigan Medical School as Chair of Pathology.

 Dr. Parkos has a career-long interest in basic mechanisms of inflammation, beginning with studies that were among the first to define the molecular basis of Chronic Granulomatous Disease, a human condition that results from defects in oxidant-mediated killing by innate immune cells (neutrophils), and then extended to studies of the biology and molecular basis of interactions between leukocytes with epithelial cells. He has a distinguished track record in these areas and, for the past 20 years, has been a major contributor in modeling the process of leukocyte transepithelial migration and effects on epithelial barrier function as it relates to mucosal inflammation and inflammatory bowel disease. His work has defined key differences and similarities between the processes of leukocyte migration across vascular endothelium and migration across mucosal epithelial barriers. He has applied state-of-the-art molecular and protein approaches to complex cell biological systems and identified a number of epithelial and neutrophil proteins that play critical roles in mucosal inflammation including CD11b/CD18, CD47, SIRPï?¡, and, most recently, specific members of the JAM family of proteins. Over the past several years, he has extended his studies to in-vivo and ex-vivo animal models of inflammation that have provided key insights into the relationship between epithelial permeability and pathologic versus homeostatic inflammatory responses.