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Published ahead of print on July 18, 2003, doi:10.1165/rcmb.2003-0091OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 3, March 2004, 271-279

A more recent version of this article appeared on March 1, 2004
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Submitted on March 19, 2003
Revised on June 30, 2003

Surfactant Protein-D, A Mediator of Innate Lung Immunity, Alters the Products of NO Metabolism

Elena N Atochina1, Michael F Beers1, Samuel Hawgood2, Francis Poulain3, Christiana Davis4, Trevor T Fusaro4, and Andrew J Gow5*

1 Pulmonary and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, PA, USA, 2 Cardiovascular Research Institute, University of California at San Francisco, San Francisco, CA, USA, 3 Pediatrics, University of California at San Francisco, San Francisco, CA, USA; Cardiovascular Research Institute, University of California at San Francisco, San Francisco, CA, USA, 4 Neonatology, Children's Hospital of Philadelphia, Philadelphia, PA, USA, 5 Pediatrics, University of Pennsylvania School of Medicine, Philadelphia, PA, USA; Neonatology, Children's Hospital of Philadelphia, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: Gow{at}email.chop.edu.

Surfactant Protein D (SP-D), a 43 kDa multifunctional collagen-like lectin, is synthesized and secreted by the airway epithelium. SP-D knockout (SP-D (-/-)) mice exhibit an increase in the number and size of airway macrophages, peribronchiolar inflammation, increases in metalloproteinase activity, and development of emphysema. Nitric oxide (NO) is involved in a variety of signaling processes, and since altered NO metabolism has been observed in inflammation, we hypothesized that alterations in its metabolism would underlie the proinflammatory state observed in SP-D deficiency. Examination of the bronchial alveolar lavage (BAL) from SP-D (-/-) mice reveals a significant increase in protein and phospholipid content and total cell count. NO production and iNOS expression were increased in the BAL, however, there was a decline in S-nitrosothiol (SNO) content in the BAL and a loss of SNO immunoreactivity within the tissue. This decline in SNO was accompanied by an increase in nitrotyrosine staining. We conclude that inflammation which occurs in SP-D deficiency results in an incre ase in NO production and a shift in the chemistry and targets of NO. We speculate that the proinflammatory response due to SP-D deficiency results, in part, from a disruption of NO mediated signaling within the innate immune system.




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