Published ahead of print on May 5, 2005, doi:10.1164/rccm.200501-109OC
American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 225-232, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200501-109OC
Surfactant Palmitoylmyristoylphosphatidylcholine Is a Marker for Alveolar Size during Disease
Ross Ridsdale*,
Matthias Roth-Kleiner*,
Frank D'Ovidio,
Sharon Unger,
Man Yi,
Shaf Keshavjee,
A. Keith Tanswell and
Martin Post
Canadian Institutes of Health Research Group in Lung Development, Lung Biology Program, Hospital for Sick Children Research Institute; Institute of Medical Sciences, and Toronto Lung Transplant Program, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada; and Division of Neonatology, Department of Pediatrics, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland
Correspondence and requests for reprints should be addressed to Martin Post, Ph.D., Lung Biology Program, Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada. E-mail: martin.post{at}sickkids.ca
Two common lung-related complications in the neonate are respiratory distress syndrome, which is associated with a failure to generate low surface tension at the air–liquid interface because of pulmonary surfactant insufficiency, and bronchopulmonary dysplasia (BPD), a chronic lung injury with reduced alveolarization. Surfactant phosphatidylcholine (PC) molecular species composition during alveolarization has not been examined. Mass spectrometry analysis of bronchoalveolar lavage fluid of rodents and humans revealed significant changes in surfactant PC during alveolar development and BPD. In rats, total PC content rose during alveolarization, which was caused by an increase in palmitoylmyristoyl-PC (16:0/14:0PC) concentration. Furthermore, two animal models of BPD exhibited a specific reduction in 16:0/14:0PC content. In humans, 16:0/14:0PC content was specifically decreased in patients with BPD and emphysema compared with patients without alveolar pathology. Palmitoylmyristoyl-PC content increased with increasing intrinsic surfactant curvature, suggesting that it affects surfactant function in the septating lung. The changes in acyl composition of PC were attributed to type II cells producing an altered surfactant during alveolar development. These data are compatible with extracellular surfactant 16:0/14:0PC content being an indicator of alveolar architecture of the lung.
Key Words: alveolar size • bronchopulmonary dysplasia • development • emphysema • surfactant phosphatidylcholine
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