Research Papers: Immunology:
Decreased severity of collagen antibody and lipopolysaccharide-induced arthritis in human IL-32β overexpressed transgenic mice
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Mi Hee Park1,*, Do-Young Yoon2,*, Jung Ok Ban3, Dae Hwan Kim1, Dong Hun Lee1, Sukgil Song1, Youngsoo Kim1, Sang-Bae Han1, Hee Pom Lee1 and Jin Tae Hong1
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
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
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.
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