AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (September 5, 2003). doi:10.1152/ajplung.00427.2002
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
286/1/L129    most recent
00427.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Alcorn, J. F.
Right arrow Articles by Wright, J. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Alcorn, J. F.
Right arrow Articles by Wright, J. R.
Submitted on December 13, 2002
Accepted on September 4, 2003

Surfactant Protein A Inhibits Alveolar Macrophage Cytokine Production by a CD14 - Independent Pathway

John F. Alcorn1 and Jo Rae Wright1*

1 Department of Cell Biology, Duke University Medical Center, Durham, NC, USA

* To whom correspondence should be addressed. E-mail: j.wright{at}cellbio.duk.edu.

The lung collectin surfactant protein - A (SP-A) has both anti-inflammatory and pro-phagocytic activities. We and others have previously shown that SP-A inhibits the macrophage production of TNF-{alpha} stimulated by the gram negative bacterial component lipopolysaccharide (LPS). We propose that SP-A decreases the production of proinflammatory cytokines by alveolar macrophages via a CD14 independent mechanism. SP-A inhibited LPS-simulated TNF-{alpha} production in rat and mouse macrophages in the presence and absence of serum (72% and 42% inhibition, respectively). In addition, SP-A inhibited LPS-induced mRNA levels for TNF-{alpha}, IL-1{alpha}, and IL-1{beta} as well as NF-{kappa}B DNA binding activity. SP-A also diminished ultra-pure LPS stimulated TNF-{alpha} produced by wild-type and CD14 null mouse alveolar macrophages by 58 and 88%, respectively. Additionally, SP-A inhibited TNF-{alpha} stimulated by phorbol ester myristate (PMA) in both wild-type and TLR4 mutant macrophages. These data suggest that SP-A inhibits inflammatory cytokine production in a CD14 independent manner and also by mechanisms independent of the LPS signaling pathway.




This article has been cited by other articles:


Home page
 Biol. Reprod.Home page
I. Garcia-Verdugo, Z. Tanfin, E. Dallot, M.-J. Leroy, and M. Breuiller-Fouche
Surfactant Protein A Signaling Pathways in Human Uterine Smooth Muscle Cells
Biol Reprod, August 1, 2008; 79(2): 348 - 355.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
J. Zhang, S. D. Tachado, N. Patel, J. Zhu, A. Imrich, P. Manfruelli, M. Cushion, T. B. Kinane, and H. Koziel
Negative regulatory role of mannose receptors on human alveolar macrophage proinflammatory cytokine release in vitro
J. Leukoc. Biol., September 1, 2005; 78(3): 665 - 674.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
B. Janic, T. M. Umstead, D. S. Phelps, and J. Floros
Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation
Am J Physiol Lung Cell Mol Physiol, February 1, 2005; 288(2): L317 - L325.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Cell Mol. Bio.Home page
Y. Wu, S. Adam, L. Hamann, H. Heine, A. J. Ulmer, U. Buwitt-Beckmann, and C. Stamme
Accumulation of Inhibitory {kappa}B-{alpha} as a Mechanism Contributing to the Anti-Inflammatory Effects of Surfactant Protein-A
Am. J. Respir. Cell Mol. Biol., December 1, 2004; 31(6): 587 - 594.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2003 by the American Physiological Society.