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Articles in PresS, published online ahead of print May 3, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00071.2002
Submitted on February 28, 2002
Accepted on April 25, 2002
1 Department of Medicine, University At Buffalo, Buffalo, NY, USA; The Center for Microbial Pathogenesis, University at Buffalo, Buffalo, NY, USA
2 Department of Pediatrics, University at Buffalo, Buffalo, NY, USA
3 The Center for Microbial Pathogenesis, University at Buffalo, Buffalo, NY, USA; Department of Anesthesiology, University at Buffalo, Buffalo, NY, USA
4 Department of Microbiology, University at Buffalo, Buffalo, NY, USA; The Center for Microbial Pathogenesis, University at Buffalo, Buffalo, NY, USA; Department of Anesthesiology, University at Buffalo, Buffalo, NY, USA
5 Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA
6 Department of Pediatrics, University of Rochester, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: trusso{at}acsu.buffalo.edu.
An in vivo rat model was utilized to evaluate the effects of Escherichia coli pneumonia on lung function and surfactant content and aggregation in bronchoalveolar lavage (BAL). Total extracellular surfactant based on phospholipid and apoprotein levels in BAL was increased in infected rats compared to controls. BAL phospholipid content in infected rats correlated with the severity of alveolar-capillary leak as reflected in lavage protein levels (R2 = 0.908, P < 0.0001). Western blotting showed that levels of the surfactant proteins, SP-A and SP-D, in BAL were significantly increased in both large and small aggregate fractions at 2 and 6 hours post-instillation of E. coli. SP-B was also increased at these times in the large aggregate fraction of BAL, while SP-C levels were increased at 2 hrs and decreased at 6 hrs relative to controls. The small to large (S/L) aggregate ratio (a marker inversely proportional to surfactant function) was increased in infected rats with >50 mg total BAL protein. There was a significant correlation (R2 = 0.885, P < 0.0001) between increasing S/L ratio in BAL and pulmonary damage assessed by total protein. Control (n=6) and experimental (n=12) rats with <50 mg total BAL protein had mean S/L ratios of 0.94 ±0.08 (S.E.) and 0.99 ±0.07, respectively. Rats with >50 mg BAL protein (n=9) had an S/L ratio of 2.57 ± 0.68 (P = 0.015 relative to controls). Pulmonary volumes, compliance, and oxygen exchange were significantly decreased in infected rats with >50 mg total BAL protein, consistent with surfactant dysfunction. In vitro surface cycling studies with calf lung surfactant extract suggested that bacterial-derived factors may have contributed, at least in part, to the alterations in surfactant aggregates seen in vivo.
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