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1 Department of internal Medicine/Pulmonary and Critical Care Medicine, Wake Forest University Schooll of Medicine, Winston-Salem, NC, USA
2 Department of internal Medicine/Pulmonary and Critical Care Medicine, Wake Forest University Schooll of Medicine, Winston-Salem, NC, USA; Department of Internal Medicine/Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA
3 Department of Publich Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Department of internal Medicine/Pulmonary and Critical Care Medicine, Wake Forest University Schooll of Medicine, Winston-Salem, NC, USA
4 Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Department of internal Medicine/Pulmonary and Critical Care Medicine, Wake Forest University Schooll of Medicine, Winston-Salem, NC, USA
5 Department of Internal Medicine/Molecular Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Department of internal Medicine/Pulmonary and Critical Care Medicine, Wake Forest University Schooll of Medicine, Winston-Salem, NC, USA
* To whom correspondence should be addressed. E-mail: dhite{at}wfubmc.edu.
In asthma, inflammation-mediated surfactant dysfunction contributes to increased airway resistance, but the mechanisms for dysfunction are not understood. To test mechanisms that alter surfactant function, atopic asthmatics underwent endobronchial antigen challenge and
bronchoalveolar lavage (BAL). BAL fluids were sequentially separated into cells, surfactant and supernatant and multiple endpoints were analyzed. Each endpoint's unique relationship to surfactant dysfunction was determined. Our results demonstrate that minimum surface tension (
min) of surfactant after antigen challenge was significantly increased with a spectrum of responses that included dysfunction in 6 of 13 asthmatics. Antigen challenge significantly altered the partitioning
of surfactant phospholipid measured as a decreased ratio of large surfactant aggregates (LA) to small surfactant aggregates (SA), LA/SA ratio. Phosphatidylglycerol (PG) was significantly reduced in the LA of the dysfunctional asthmatic BALs. There was a corresponding significant increase in the ratio of phosphatidylcholine (PC) to PG, which strongly correlated with both increased min and decreased LA/SA. Altered surfactant phospholipid properties correlated with surfactant dysfunction as well or better than either increased eosinophils or protein. Secretory phospholipase activity,
measured in vitro, increased after antigen challenge and may explain the decrease in surfactant PG. In summary, alteration of phospholipids, particularly depletion of PG, in the LA of surfactant may be an important mechanism in asthma-associated surfactant dysfunction.
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