Decreased severity of collagen antibody and lipopolysaccharide-induced arthritis in human IL-32β overexpressed transgenic mice

// Mi Hee Park 1,* , Do-Young Yoon 2,* , Jung Ok Ban 3 , Dae Hwan Kim 1 , Dong Hun Lee 1 , Sukgil Song 1 , Youngsoo Kim 1 , Sang-Bae Han 1 , Hee Pom Lee 1 and Jin Tae Hong 1 1 College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea 2 Department of Bioscience and Biotechnology, Laboratory of Cell Biology and Immunobiochemistry, Bio/Molecular Informatics Center, Konkuk University, Hwayang-dong 1, Gwangjin-gu, Seoul, Republic of Korea 3 Osong Medical Innovation Foundation, Osongsaengmyeong 1-ro, Osong-eup, Cheongwon-gun, Chungbuk, Republic of Korea * The authors have contributed equally to this work Correspondence to: Jin Tae Hong, email: // Hee Pom Lee, email: // Keywords : IL-32β, anti-arthritis, anti-inflammatory cytokine, Immunology and Microbiology Section, Immune response, Immunity Received : August 10, 2015 Accepted : October 01, 2015 Published : October 19, 2015 Abstract Interleukin (IL)-32, mainly produced by T-lymphocytes, natural killer cells, epithelial cells, and blood monocytes, is dominantly known as a pro-inflammatory cytokine. However, the role of IL-32 on inflammatory disease has been doubtful according to diverse conflicting results. This study was designed to examine the role of IL-32β on the development of collagen antibody (CAIA) and lipopolysaccharide (LPS)-induced inflammatory arthritis. Our data showed that the paw swelling volume and clinical score were significantly reduced in the CAIA and LPS-treated IL-32β transgenic mice compared with non-transgenic mice. The populations of cytotoxic T, NK and dendritic cells was inhibited and NF-κB and STAT3 activities were significantly lowered in the CAIA and LPS-treated IL-32β transgenic mice. The expression of pro-inflammatory proteins was prevented in the paw tissues of CAIA and LPS-treated IL-32β transgenic mice. In addition, IL-32β altered several cytokine levels in the blood, spleen and paw joint. Our data indicates that IL-32β comprehensively inhibits the inflammation responses in the CAIA and LPS-induced inflammatory arthritis model.