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Published ahead of print on May 13, 2004, doi:10.1165/rcmb.2003-0438OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 3, September 2004, 330-336

A more recent version of this article appeared on September 1, 2004
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Submitted on December 8, 2003
Revised on May 13, 2004

A20 inhibits Toll-like receptor 2 and 4-mediated interleukine-8 synthesis in airway epithelial cells

Yasuhiro Gon1, Yasukiyo Asai2, Shu Hashimoto2*, Kenji Mizumura2, Itsuro Jibiki2, Tatsuya Machino2, Chisei Ra3, and Takashi Horie2

1 First Department of Internal Medicine, Nihon University School of Medicine, Itabashi-Ku, Tokyo, Japan; Division of Molecular Cell Immunology and Allergology, Nihon University, Itabashi-Ku, Tokyo, Japan, 2 First Department of Internal Medicine, Nihon University School of Medicine, Itabashi-Ku, Tokyo, Japan, 3 Division of Molecular Cell Immunology and Allergology, Nihon University, Itabashi-Ku, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: shuh{at}med.nihon-u.ac.jp.

The zinc finger protein A20 is encoded by an immediate early response gene and acts as an inhibitor of NF-{kappa}B-dependent gene expression induced by different stimuli, including tumor-necrosis factor-{alpha} (TNF-{alpha})and interleukin 1{beta} (IL-1{beta}). Toll-like receptor 2 (TLR2) and TLR4 have been found to transduce, respectively, peptidoglycan (PGN) and lipopolysaccharide (LPS) signals for the activation of NF-{kappa}B and the production of inflammatory cytokines. Here, we have examined the role of A20 in TLR-mediated NF-{kappa}B-dependent gene expression in human airway epithelial cells (AECs). Stimulation with LPS and PGN resulted in a significant increase in the level of A20 mRNA in primary cultured AECs and in NCI-H292 AECs. LPS and PGN induced activation of the IL-8 promoter both in NCI-H292 AECs and in HEK293 cells expressing either TLR2 or TLR4 plus MD-2. Dominant-negative myeloid differentiation protein (MyD88) and a mutant form of I{kappa}B{alpha} attenuated this PGN- or LPS-induced activation of the IL-8 promoter. Furthermore, overexpression of A20 inhibited activation of both NF-{kappa}B and the IL-8 promoter by PGN or LPS in these cells. Taken together, our results suggest that A20 may function as a negative regulator of TLR-mediated inflammatory responses in the airway, thereby protecting the host against harmful overresponses to pathogens.




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