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Am J Physiol Lung Cell Mol Physiol (July 7, 2002). doi:10.1152/ajplung.00118.2002
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Articles in PresS, published online ahead of print July 3, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00118.2002
Submitted on April 19, 2002
Accepted on June 29, 2002

Sequential targeted deficiency of surfactant proteins A and D leads to progressive alveolar lipoproteinosis and emphysema

Samuel Hawgood1*, Matthias Ochs2, Anja Jung2, Jennifer Akiyama1, Lennell Allen1, Cindy Brown1, Jess Edmondson1, Stacey Levitt1, Elaine Carlson1, Anne Marie Gillespie1, Angela Villar1, Charles J. Epstein1, and Francis R. Poulain1

1 Department of Pediatrics, University of California San Francisco, San Francisco, California, USA
2 Department of Anatomy, University of Gottingen, Gottingen, Germany

* To whom correspondence should be addressed. E-mail: hawgood{at}itsa.ucsf.edu.

Surfactant proteins A and D (SP-A and SP-D) are members of the collectin protein family. Mice singly deficient in SP-A and SP-D have distinct phenotypes. Both have altered inflammatory responses to microbial challenges. To further investigate the functions of SP-A and SP-D in vivo we developed mice deficient in both proteins by sequentially targeting the closely linked genes in embryonic stem cells using graded resistance to G418. There is a progressive increase in bronchoalveolar lavage phospholipid, protein, and macrophage content through 24 weeks of age. The macrophages from doubly deficient mice express high levels of the matrix metalloproteinase, MMP-12 and develop intense but patchy lung inflammation. Stereological analysis demonstrates significant airspace enlargement and destruction of alveolar walls consistent with emphysema. These changes qualitatively resemble the lung pathology seen in SP-D deficient mice. These doubly deficient mice will be useful in dissecting the potential overlap in function between SP-A and SP-D in host defense.




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