|Institution||College of Medicine|
|Address||500 University Drive, Hershey, PA 17033|
Associate Proffesor of Pediatrics
1988, B.S.(honors), Biochemical and Biophysical Sciences, University of Houston Honors College, Houston, TX
1992, Ph.D., Chemistry, University of South Carolina, Columbia, SC
1992-1994, Post-Doctoral Fellowship in Biochemistry, Vanderbilt University School of Medicine, Nashville, TN
1994-1997, Post-doctoral Fellowship in Pulmonary Biology and Pediatrics, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH
The long-term goal of my research is to elucidate the role of pulmonary surfactant in perinatal development of the pulmonary immune system, lung host defense, inflammation, and injury. Alveolar type II epithelial cells produce surfactant, a complex of lipids and proteins lining the alveolar surface. Surfactant is critical for both respiratory gas exchange and the immunological integrity of the lower respiratory tract. Surfactant dysfunction thwarts the ability of alveolar macrophages to fight infection and, furthermore, to properly initiate, develop, and cease inflammatory reactions to infectious organisms and endogenous insults. Fundamental research on lung surfactant is an urgently needed and largely untapped resource in understanding, diagnosis, and treatment of chronic inflammation, acute lung injury, neonatal and adult respiratory distress syndromes, and pneumonia caused by pathogenic and drug-resistant organisms.
Surfactant modifies the ability of alveolar macrophages and type II epithelial cells to maintain immunological homeostasis avoiding inappropriate inflammatory reactions by innocuous antigens in the air we breathe. Surfactant contains the microbial binding proteins SP-A and SP-D which recognize and mediate clearance of pathogenic microorganisms by alveolar macrophages. During infection, SP-A and SP-D regulate the timing, magnitude, and resolution of inflammation. In the absence of infection, SP-A and SP-D suppress unnecessary activation of antigen-experienced lymphocytes and other immune cells in the lower respiratory tract. My research over the last 15 years has defined receptor-mediated mechanisms through which surfactant components modulate inflammatory, immune, and metabolic functions of alveolar macrophages and type II epithelial cells.
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