Research in my laboratory focuses in understanding the basic mechanisms responsible for acute lung injury and repair and to identify strategies to prevent or minimize this injury. Current areas of research include:
Viral induced injury to the mammalian alveolar epithelium. Influenza (flu) is a contagious respiratory illness caused by flu viruses, leading to an estimated 36,000 deaths every year in the United States alone, with the potential for at least a tenfold increase in epidemic and pandemic scenarios. Respiratory Syncytial Virus (RSV) is a member of the pneumovirus genus of the paramyxoviridae, and has a negative-sense, non-segmented, single-stranded RNA genome. It is the most common cause of lower respiratory tract disease in infants and children worldwide, is a frequent initiator of acute asthma exacerbations in young children, and has a disease impact comparable to that of non-pandemic influenza A in the elderly. We are currently using a variety of biophysical, molecular biology and physiological techniques to assess the basic mechanisms by which viral proteins and active replicating viruses interact with and modulate key functions of the alveolar epithelium both in vitro and in vivo. Results of these studies help us formulate new strategies for decreasing rhinorrhea and pulmonary edema, common consequences of viral infections.
Developing countermeasures against oxidant gases. The halogens chlorine (Cl2) and bromine (Br2) are produced in large quantities throughout the world and used extensively in various manufacturing processes and the sanitation of water. They are very reactive gases and pose significant threat to public health when released into the atmosphere in large quantities during transportation and industrial accidents as well as acts of terrorism. When inhaled, Cl2 and Br2 hydrolyze to form hypochlorous (HOCl) and hypobromous (HOBr) acids and their conjugate bases (OCl-, OBr-) respectively, which react with proteins, plasmalogen lipids as well as components of the lung extracellular matrix. We are conducting physiological, biochemical, morphological and biophysical studies to understand the basic mechanisms by which inhalation of Cl2 and Br2 damages the lungs and systemic organs; these mechanistic studies drive the development of specific countermeasures which when administered post exposure diminish morbidity and mortality