Dr. Thomas Braciale serves as the Interim Director of the Beirne B. Carter Center for Immunology Research. Dr. Braciale received his B.S. in Biology from St. Joseph’s College and his MD and PhD from the University of Pennsylvania. He is currently Professor of Pathology and Molecular Medicine.
My laboratory has had a long-standing interest in understanding the host immune response to respiratory virus infection with particular emphasis on the major human respiratory pathogen Influenza virus. Our previous research has included defining the contribution of respiratory tract dendritic cells in initiating the development of the adaptive immune response following influenza infection, as well as the contribution of activated influenza specific effector CD8+ and CD4+ T cells and inflammatory monocytes/macrophages in orchestrating virus clearance, and in the development of lung injury during and following virus clearance from the respiratory tract. More recently, we have begun the analysis of the role of lung resident alveolar macrophages in regulating the susceptibility of airway epithelial cells to influenza infection. We have found that this innate immune cell type plays a critical role in determining the extent of infection of alveolar epithelial cells, the lung cells involved in oxygen exchange. Current evidence suggests that one function of alveolar macrophages during influenza infection is to control the expression and action of a subclass of arachodontic acid metabolites, the cysteinyl leukotrienes. It is these lipid mediators that directly regulate the susceptibility of airway epithelial cells to influence infection. Furthermore, blocking the synthesis or action of cysteinyl leukotrienes in the infected lungs markedly reduces the severity of influenza infection. Overall these data suggest novel strategies to decrease morbidity and mortality in infection with influenza and possibly with SARS Cov-2.