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In mouse models, those “knocked out” for the fatty acid oxidation (FAO) enzyme LCAD demonstrate reduced lung function. Our research team hypothesizes that LCAD and the FAO pathway are involved in synthesizing and secreting pulmonary surfactant in a specialized lung cell known as the type II pneumocyte. Surfactant is a mixture of phospholipids and proteins that reduces surface tension in the lung. This effect is necessary to prevent the collapse of the alveoli and promote gas exchange. LCAD knockout mice have reduced amounts of surfactant lipids and an altered phospholipid composition. Preliminary studies show an increased susceptibility to infection by influenza. Efforts are underway to determine the molecular mechanisms behind these changes.
Eric Goetzman, PhD
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UPMC Children’s Hospital of Pittsburgh
One Children’s Hospital Way
4401 Penn Ave.
Pittsburgh, PA 15224
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