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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.

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

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.

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