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1 Centre for critical Illness Research, Lawson Health Research Institute, Room G454, London, Canada; Physiology and Pharmacology, The university of Western Ontario, London, Canada
2 Centre for Critical Illness research, Lawson Health Research Institute, London, Canada; Physiology and Pharmacology, The university of Western Ontario, London, Canada
3 Physiology and Pharmacology, The university of Western Ontario, London, Canada
4 Centre for Critical Illness research, Lawson Health Research Institute, London, Canada
5 Division of Respirology, St. Joseph's Health Center, London, Canada; Centre for Critical Illness research, Lawson Health Research Institute, London, Canada; Physiology and Pharmacology, The university of Western Ontario, London, Canada; Medicine, The University of Western Ontario, London, Canada
6 Centre for Critical Illness research, Lawson Health Research Institute, London, Canada; Physiology and Pharmacology, The university of Western Ontario, London, Canada; Medicine, The University of Western Ontario, London, Canada
* To whom correspondence should be addressed. E-mail: rveldhui{at}uwo.ca.
Pulmonary surfactant is a lipid-protein material that is essential for normal lung function. Maintaining normal and consistent alveolar amounts of surfactant is in part dependent on clearance of surfactant by alveolar macrophages (AM). The current study utilized a rat model of AM depletion to determine the impact on surfactant pool sizes and function over time. Male Sprague-Dawley rats were anesthetized and intratracheally instilled with PBS-liposomes (PBS-L) or Dichloromethylene diphosphonic acid (DMDP) containing lipisomes (DMDP-L) and were sacrificed at various timepoints up to 21 days for compliance measurements, AM cell counts and surfactant analysis. AM numbers were significantly decreased 1, 2, and 3 days after instillation in DMDP-L versus PBS-L, with 72% depletion at 3 days. AM numbers returned to normal levels by 5 days. In DMDP-L rats, there was a rapid increase in surfactant-phospholipid pools, showing a 9-fold increase in the amount of surfactant in the lavage 3 days after liposome instillation. Surfactant accumulation progressed up to 7 days, with pools normalizing by 21 days. The increase in surfactant was due to increases in both subfractions of surfactant, the large (LA) and small (SA) aggregates. Surfactant protein A levels, relative to LA phospholipids, were not increased. There was a decreased extent of surfactant conversion in vitro for LA from DMDP-L rats compared controls. It is concluded that the procedure of AM depletion significantly affects surfactant metabolism. The increased endogenous surfactant must be considered when utilizing the AM depletion model to study the role of these cells during lung insults.
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