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Published ahead of print on August 12, 2004, doi:10.1165/rcmb.2004-0003OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 587-594

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Submitted on January 12, 2004
Revised on August 12, 2004

Accumulation of I{kappa}B-{alpha} as a Mechanism Contributing to the Anti-inflammatory Effects of SP-A

Yingda Wu1, Stefanie Adam2, Lutz Hamann3, Holger Heine4, Artur J Ulmer4, Ute Buwitt-Beckmann4, and Cordula Stamme5*

1 Department of Anesthesiology, First Affiliated Hospital of Medicine College, Zhejiang University, Zhejiang, Hangzhou, China; Department of Immunochemistry and Biochemical Microbiology, Research Center Borstel, Borstel, Germany, 2 Department of Immunochemistry and Biochemical Microbiology, Research Center Borstel, Borstel, Germany, 3 Department of Microbiology and Hygiene, Humboldt University Berlin, Berlin, Germany, 4 Department of Immunology and Cell Biology, Research Center Borstel, Borstel, Germany, 5 Department of Immunochemistry and Biochemical Microbiology, Research Center Borstel, Borstel, Germany; Department of Anesthesiology, University of Lubeck, Lubeck, Germany

* To whom correspondence should be addressed. E-mail: cstamme{at}fz-borstel.de.

The collectin surfactant protein A (SP-A) has been implicated in multiple immunoregulatory functions of innate pulmonary host defense via modulating immune responses both in vitro and in vivo. The present study aimed to investigate mechanisms responsible for the anti-inflammatory effects of human (hu) SP-A on the inhibitory kappa B (I{kappa}B-{alpha})/nuclear factor-{kappa}B (NF-{kappa}B) signaling pathway in alveolar macrophages (AMs). Initially performed CD25 expression analysis of CD14/huToll-like receptor 4 Chinese hamster ovary reporter cells by flow cytometry demonstrated that SP-A alone does not induce any NF-{kappa}B-dependent CD25 expression in these cells. In AMs, SP-A pretreatment caused a marked inhibition of LPS-induced NF-{kappa}B activation independent of the LPS chemotype used as determined by electrophoretic mobility shift assay. Western blot analysis revealed that SP-A by itself increased the protein expression of I{kappa}B-{alpha}, the predominant regulator for rapidly induced NF-{kappa}B, in a dose- and time-dependent manner without enhancing I{kappa}B-{alpha} messenger RNA as determined by reverse transcription-polymerase chain reaction. SP-A did not interfere with LPS-induced serine 32 phosphorylation of I{kappa}B-{alpha} but significantly enhanced I{kappa}B-{alpha} abundance under LPS-coupled conditions. The data suggest that anti-inflammatory effects of SP-A on LPS-challenged AMs are associated with a SP-A-mediated direct modulation of the I{kappa}B-{alpha} turnover in these cells.




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