Dr. Patrick Flood

Biography

Dr. Patrick Flood received his PhD degree in Immunology from the University of Chicago in 1980 under the direction of Dr. Hans Schreiber. Research from his dissertation demonstrated a crucial role for T lymphocytes in the protective immune response to skin cancer induced by ultraviolet light, and suggested a new approach to immunotherapy for treating malignant diseases. Dr. Flood completed his postdoctoral fellowship under the direction of the late Dr. Richard Gershon at the Yale University, where he studied immune regulation and cancer. Dr. Flood then received a joint appointment to the faculty in the Department of Pathology at the Yale University School of Medicine and as an Investigator at the Howard Hughes Medical Institute at Yale University. Dr. Flood moved to the University of North Carolina at Chapel Hill in 1988, where he served on the faculty of Periodontology and Immunology for 25 years. During his time at the University of North Carolina, Dr. Flood served as Program Director and Director of the Pathogenesis Training Track for the Graduate Curriculum in Oral Biology, Associate Dean for Research and Director of the Dental Research Center at the School of Dentistry, Director of the Comprehensive Center for Inflammatory Disorders, and as a member of the Lineberger Comprehensive Cancer Center, the Carolina Center for Genome Sciences, and the Neuroscience Graduate Training Program at the University of North Carolina. Dr. Flood began his appointment at the School of Dentistry, University of Alberta in September, 2012. Dr. Flood’s primary research is in the field of innate immunity and inflammation, with an emphasis on treatment of chronic inflammatory disorders. One goal of his research is to understand the mechanisms by which innate immune responses regulate oral inflammation. The central goal of this research is to understand the role of innate immune cells, particularly macrophages, in the initiation of regulation of inflammatory responses to Periodontal pathogens, and the role of adaptive immune cells and products, particularly Treg cells, in the regulating these responses. A second area of emphasis is neuroimmunology, which studies the relationship between responses of the Nervous System and the Immune System. The central goal of his research in this area is to understand how immune cells are activated and regulated within the Central Nervous System (CNS), and what role these cells play in sensory responses and in autoimmune diseases affecting sensory perception within the CNS. Investigation centers on the role of the microglia, the central inflammatory cell of the CNS, and its relationship to chronic inflammation. The research investigates the different pathways of activation of the microglia, the role of the microglia in sensory responses, and the role of stress responses initiated through b2-adrenergic receptors (b2AR) in activating and regulating the response of the microglia. He is currently investigating the mechanism by activated microglia mediate neurotoxicity using an in vitro and in vivo models of Parkinson’s disease (PD), and investigating the role of inflammatory mediator production and oxidative stress responses in the progression of disease. This research also has a strong emphasis on understanding the role of specific pathways involved in inflammation, and in developing therapeutics targeted to specific critical inflammatory pathways and mediators involved in chronic inflammatory response in gingivitis and periodontitis. Dr. Flood has published over 150 original scientific publications, mentored over 80 graduate and postdoctoral trainees, given numerous scientific presentations at national and international meetings, and served as a reviewer and/or editor for over 20 journals. He is currently serving as the Associate Chair of Research in the School of Dentistry.

Research Interest

The regulation of macrophages in chronic inflammatory conditions Identification of new therapeutic anti-inflammatory strategies for the treatment of periodontal and other chronic inflammatory conditions Mechanisms of conversion of macrophages from pro-inflammatory to anti-inflammatory phenotypes Current projects Development of effective new anti-inflammatory therapeutics for the treatment of chronic inflammation. Our research looks at the different pathways of activation of the macrophage and the microglia, to develop targets to those pathways for the treatment of Periodontal Disease (PerioD) and Parkinson’s disease (PD), our two models of inflammation. We have developed several effective treatments which stop and actually reverse neurodegeneration in several animal models of PD, targeting the NF-kB and MAP-K signaling pathways. Studying the role of stress responses initiated through b2-adrenergic receptors (b2AR) in activating and regulating the response of the microglia. We are currently investigating the mechanism by activated microglia mediate neurotoxicity using an in vitro and in vivo model of Parkinson’s Disease (PD), Studying the role of oxidative stress in the destruction of dopaminergic neurons. We have demonstrated the importance of the oxidative stress response mediated through NADPH oxidase in dopaminergic neuronal destruction, and are currently targeting this pathway as a treatment for PerioD and PD. Studying the regulation of M1 and M2 cells in inflammatory lesions. We are currently studying the basic mechanism of M1 and M2 signaling in macrophages, and are developing treatments that target these mechanisms to convert M1 pro-inflammatory cells into M2 anti-inflammatory cells as a treatment for chronic inflammation.