Published ahead of print on September 4, 2003, doi:10.1165/rcmb.2003-0246OC
American Journal of Respiratory Cell and Molecular Biology. Vol. 30, pp. 319-325, 2004
© 2004 American Thoracic Society DOI: 10.1165/rcmb.2003-0246OC
Role of Surfactant Protein-A in Nitric Oxide Production and Mycoplasma Killing in Congenic C57BL/6 Mice
Judy M. Hickman-Davis,
Julie Gibbs-Erwin,
J. Russell Lindsey and
Sadis Matalon
Departments of Anesthesiology, Genomics and Pathobiology, and Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama
Address correspondence to: Dr. Sadis Matalon, Department of Anesthesiology, University of Alabama at Birmingham, UAB Dept. of Anesthesiology, 1530 3rd Ave. South, Birmingham, AL 35294-2172. E-mail: Sadis.Matalon{at}ccc.uab.edu
We generated congenic surfactant protein A (SP-A)deficient (SP-A[-/-]) mice on the mycoplasma resistant C57BL/6 background (B6.SP-A[-/-]) and characterized their response to mycoplasma infection in comparison to C57BL/6 (B6) mice. B6.SP-A(-/-) mice infected with 106 colony-forming units (cfu) of Mycoplasma pulmonis had significantly higher bacterial lung loads than B6 mice at 72 h postinfection (p.i.). At the higher infection dose of 107, B6.SP-A(-/-) mice had significantly higher lung cfu at 24 h; however, no difference in mycoplasma cfu was observed between B6 and B6.SP-A(-/-) mice at 48 and 72 h p.i. We found that uninfected B6 mice had lower bronchoalveolar lavage nitrite (NO2-) and nitrate (NO3-) levels as compared with B6.SP-A(-/-) mice. On the other hand, infection of B6 mice with mycoplasmas resulted in significantly higher bronchoalveolar lavage NO2- and NO3- as compared with B6.SP-A(-/-) mice. These data indicate that SP-A may help regulate NO production in response to a specific stimulus, i.e., suppression of NO in the absence of bacteria and increased NO in the presence of bacteria. These data indicate that the contribution of SP-A to mycoplasma killing may be limited to lower doses of pathogens.
Abbreviations: alveolar macrophage, AM acidophilic macrophage pneumonia, AMP bronchoalveolar lavage, BAL colony-forming unit, cfu interferon- , IFN- interleukin-1ß, IL-1ß monocyte chemotactic protein, MCP nitric oxide, NO polymerase chain reaction, PCR postinfection, p.i. polymorphonuclear cells, PMN surfactant protein A, SP-A tumor necrosis factor- , TNF-
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