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A20 Attenuates Allergic Airway Inflammation in Mice¹

Nam-In Kang^2,*, Ha-Yong Yoon^2,, Young-Rae Lee^2,, Minho Won, Myoung Ja Chung, Jin-Woo Park, Gang Min Hur, Hern-Ku Lee^* and Byung-Hyun Park^3,

^* Department of Immunology, Department of Biochemistry, and Department of Pathology, Medical School and Diabetes Research Center, Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea; and Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea

TNF receptor 1 can activate signaling pathways leading to the activation of NF-B. A20, an NF-B-inducible protein, negatively regulates these signaling pathways and acts as an anti-inflammatory mediator. Therefore, A20 is viewed as a potential therapeutic target for inflammatory disease. In this study, we examined the effect of A20 on an OVA-induced allergic airway inflammation model in mice. We used an adenovirus containing A20 cDNA (Ad-A20) that was delivered intratracheally before OVA challenge. Single administration of Ad-A20 reduced airway inflammatory cell recruitment and peribronchiolar inflammation and suppressed the production of various cytokines in bronchoalveolar fluid. In addition, Ad-A20 suppressed mucus production and prevented the development of airway hyperresponsiveness. The protective effect of Ad-A20 was mediated by the inhibition of the NF-B signaling pathway. Taken together, our results suggest that the development of an immunoregulatory strategy based on A20 may have therapeutic potential for the treatment of allergic asthma.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by a grant from the Ministry of Science and Technology (MoST)/Korea Science and Engineering Foundation (KOSEF) through the Diabetes Research Center at Chonbuk National University (R13-2008-005-0000-0).

² N.-I.K., H.-Y.Y., and Y.-R.L. contributed equally to this study.

³ Address correspondence and reprint requests to Dr. Byung-Hyun Park, Department of Biochemistry, Medical School, Chonbuk National University, Jeonju, Jeonbuk, Republic of Korea. E-mail address: bhpark{at}chonbuk.ac.kr

⁴ Abbreviations used in this paper: AHR, airway hyper-responsiveness; TNF-R1, TNF receptor 1; RIP, receptor interacting protein; TRAF2, TNF-associated factor 2; i.t., intratracheal; BAL, bronchoalveolar lavage; BALF, BAL fluid; Ad-A20, adenovirus expressing A20; Ad-GFP, adenovirus expressing GFP.

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