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The Proceedings of the American Thoracic Society 6:323 (2009)
© 2009 The American Thoracic Society
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Surfactant Protein A Function in Asthma Is Defective as a Modulator of Inflammation during Infection

Daniel H. Fertel1, Tony D. Church1, Ying Wang1, Hong Wei Chu2, Dennis R. Voelker2, Jo Rae Wright1 and Monica Kraft1

1 Duke University Medical Center, Durham, North Carolina; and 2 National Jewish Medical and Research Center, Denver, Colorado

Correspondence and requests for reprints should be addressed to Monica Kraft, M.D., Duke University Medical Center, DUMC 2641, Durham, NC 27710. E-mail: monica.kraft{at}duke.edu

The exaggerated inflammatory response of asthmatic epithelial cells to in-vitro challenge with Mycoplasma pneumoniae (MP) has been previously described. Surfactant protein A (SP-A) attenuates this inflammatory response in nonasthmatic epithelial cells. Hypothesis: SP-A derived from patients with asthma is less effective in modulating inflammation than SP-A from normal subjects. Methods: Airway epithelial cells from 10 subjects with asthma (FEV1: 81 ± 5% predicted) and 5 normal subjects (FEV1: 95 ± 4% predicted) were cultured. SP-A was isolated from bronchoalveolar lavage by ultracentrifugation. After 14 days at an air–liquid interface, cells were exposed to normal (NSP-A) and asthmatic SP-A (A-SPA) separately or both combined 30 minutes before exposure to MP and incubated for 48 hours. IL-8 was determined by ELISA and MUC5AC mRNA by RT-PCR. Results: MP alone significantly increased MUC5AC and IL-8 expression above negative control only in asthmatic cells (P < 0.05). NSP-A significantly decreased IL-8 and MUC5AC from both groups (P < 0.05), but ASP-A did not attenuate MUC5AC and IL-8 expression significantly in either group compared with MP alone. The combination of NSP-A and ASP-A decreased expression of both mediators to the level of uninfected control, ruling out the presence of an inhibitor (Figure). Conclusions: A-SPA failed to abrogate inflammation associated with infection, suggesting one aspect of impaired innate immunity in asthma.
Figure 1

FOOTNOTES

Supported by: PO1 HL073907–01 (M.K.), SCCOR HL-084917.

Conflict of Interest Statement: D.H.F. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. T.D.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. Y.W. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. H.W.C. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. D.R.V. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. J.R.W. received an honorarium of $1,000 for giving a talk at Kyoto University. The honorarium was from Ono Pharmaceuticals. M.K. has consulting fees from GlaxoSmithKline in 2006 and 2007. She has also received research funding in 2007, and she received consulting fees from Advisory Board participation from AstraZeneca, Merck, and Genentech in 2006 and 2007. She received research funding from Genentech and Novartis in 2006 and 2007. She also received lecture fees from Merck, AstraZeneca, and Schering for participation in their speakers' bureau in 2006 and 2007.

(Received in original form July 10, 2008; accepted in final form November 4, 2008)





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