help button home button
AJRCMB
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Published ahead of print on September 4, 2003, doi:10.1165/rcmb.2003-0246OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 3, March 2004, 319-325

A more recent version of this article appeared on March 1, 2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
2003-0246OCv1
30/3/319    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hickman-Davis, J. M
Right arrow Articles by Matalon, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hickman-Davis, J. M
Right arrow Articles by Matalon, S.

Submitted on June 27, 2003
Revised on September 2, 2003

ROLE OF SP-A IN NO PRODUCTION AND MYCOPLASMA KILLING IN CONGENIC C57BL/6 MICE

Judy M Hickman-Davis1, Julie Gibbs-Erwin1, J. Russell Lindsey2, and Sadis Matalon3*

1 Anesthesiology, University of Alabama, Birmingham, AL, USA, 2 Genomics and Pathobiology, University of Alabama, Birmingham, AL, USA, 3 Anesthesiology, University of Alabama, Birmingham, AL, USA; Genomics and Pathobiology, University of Alabama, Birmingham, AL, USA; Physiology and Biophysics, University of Alabama, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: sadis{at}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 hours postinfection (p.i.). At the higher infection dose of 107, B6.SP-A(-/-) mice had significantly higher lung CFU at 24 hours, however, no difference in mycoplasma CFU was observed between B6 and B6.SP-A(-/-) mice at 48 and 72 hours p.i. We found that uninfected B6 mice had lower BAL nitrite (NO2-) and nitrate (NO3-) levels as compared to B6.SP-A(-/-) mice. On the other hand, infection of B6 mice with mycoplasmas resulted in significantly higher BAL NO2- and NO3- as compared to 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.




This article has been cited by other articles:


Home page
 Infect. Immun.Home page
A. N. Mikerov, G. Wang, T. M. Umstead, M. Zacharatos, N. J. Thomas, D. S. Phelps, and J. Floros
Surfactant Protein A2 (SP-A2) Variants Expressed in CHO Cells Stimulate Phagocytosis of Pseudomonas aeruginosa More than Do SP-A1 Variants
Infect. Immun., March 1, 2007; 75(3): 1403 - 1412.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
J. M. Hickman-Davis, Z. Wang, G. A. Fierro-Perez, P. R. Chess, G. P. Page, S. Matalon, and R. H. Notter
Surfactant Dysfunction in SP-A-/- and iNOS-/- Mice with Mycoplasma Infection
Am. J. Respir. Cell Mol. Biol., January 1, 2007; 36(1): 103 - 113.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
C. M. Prado, E. A. Leick-Maldonado, L. Yano, A. S. Leme, V. L. Capelozzi, M. A. Martins, and I. F. L. C. Tiberio
Effects of Nitric Oxide Synthases in Chronic Allergic Airway Inflammation and Remodeling
Am. J. Respir. Cell Mol. Biol., October 1, 2006; 35(4): 457 - 465.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
I. C. Davis, E. R. Lazarowski, J. M. Hickman-Davis, J. A. Fortenberry, F.-P. Chen, X. Zhao, E. Sorscher, L. M. Graves, W. M. Sullender, and S. Matalon
Leflunomide Prevents Alveolar Fluid Clearance Inhibition by Respiratory Syncytial Virus
Am. J. Respir. Crit. Care Med., March 15, 2006; 173(6): 673 - 682.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
C.-H. Yang, J. Szeliga, J. Jordan, S. Faske, Z. Sever-Chroneos, B. Dorsett, R. E. Christian, R. E. Settlage, J. Shabanowitz, D. F. Hunt, et al.
Identification of the Surfactant Protein A Receptor 210 as the Unconventional Myosin 18A
J. Biol. Chem., October 14, 2005; 280(41): 34447 - 34457.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. Piboonpocanun, H. Chiba, H. Mitsuzawa, W. Martin, R. C. Murphy, R. J. Harbeck, and D. R. Voelker
Surfactant Protein A Binds Mycoplasma pneumoniae with High Affinity and Attenuates Its Growth by Recognition of Disaturated Phosphatidylglycerols
J. Biol. Chem., January 7, 2005; 280(1): 9 - 17.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
A. N. Mikerov, T. M. Umstead, W. Huang, W. Liu, D. S. Phelps, and J. Floros
SP-A1 and SP-A2 variants differentially enhance association of Pseudomonas aeruginosa with rat alveolar macrophages
Am J Physiol Lung Cell Mol Physiol, January 1, 2005; 288(1): L150 - L158.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
S. Matalon and J. R. Wright
Surfactant Proteins and Inflammation: The Yin and the Yang
Am. J. Respir. Cell Mol. Biol., December 1, 2004; 31(6): 585 - 586.
[Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
A. M. LeVine, J. Elliott, J. A. Whitsett, A. Srikiatkhachorn, E. Crouch, N. DeSilva, and T. Korfhagen
Surfactant Protein-D Enhances Phagocytosis and Pulmonary Clearance of Respiratory Syncytial Virus
Am. J. Respir. Cell Mol. Biol., August 1, 2004; 31(2): 193 - 199.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Crit. Care Med.
Copyright © 2003 American Thoracic Society.