Dr. Burton F. Dickey
The University of Texas MD Anderson Cancer Center
Department of Pulmonary Medicine
The principal focus of our laboratory is the molecular mechanism and pathophysiologic significance of airway mucin secretion. We use a mouse genetic approach that allows us both to gain fundamental insight into the molecular mechanism of secretion and to use mutant mice in models of pathophysiologic challenge. This work has given us knowledge of the control of normal mucin secretion, particularly by Munc18, Munc13, Syntaxin and Synaptotagmin proteins. It has also helped us understand how its dysregulation contributes to pathophysiology in disease states such as asthma and cystic fibrosis.
Epithelial Innate Immunity
Since inflammatory mediators are critical regulators of mucin production, we have also studied protective and pathologic roles of airway inflammation. This work has led to the recognition that distinct types of inflammation differentially induce mucin production, resistance to microbial infection, and promotion of epithelial carcinogenesis. Inducible resistance of airway epithelium to microbial infection has become another major interest of the laboratory, in collaboration with Scott E. Evans. Whereas Dr. Evans focuses primarily on the molecular mechanism of innate resistance, we focus on translating basic observations into a clinical therapy to prevent respiratory infection.