Decreased severity of collagen antibody and lipopolysaccharide-induced arthritis in human IL-32β overexpressed transgenic mice.
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.
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Mi Hee
MH
Park
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.
Do-Young
DY
Yoon
Osong Medical Innovation Foundation, Osongsaengmyeong 1-ro, Osong-eup, Cheongwon-gun, Chungbuk, Republic of Korea.
Jung Ok
JO
Ban
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Dae Hwan
DH
Kim
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Dong Hun
DH
Lee
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Sukgil
S
Song
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Youngsoo
Y
Kim
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Sang-Bae
SB
Han
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Hee Pom
HP
Lee
College of Pharmacy and Medical Research Center, Chungbuk National University, Osongsaengmyeong 1-ro, Osong-eup, Cheong-ju, Chungbuk, Republic of Korea.
Jin Tae
JT
Hong
D000818:Animals; D000906:Antibodies / Q000008:administration & dosage; D001168:Arthritis / Q000139:chemically induced* / Q000276:immunology*; D003094:Collagen / Q000276:immunology*; D006801:Humans; D007378:Interleukins / Q000096:biosynthesis* / Q000276:immunology*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008297:Male; D051379:Mice; D008822:Mice, Transgenic
D000906:Antibodies; C496971:IL32 protein, human; D007378:Interleukins; D008070:Lipopolysaccharides; D003094:Collagen
IL-32β; Immune response; Immunity; Immunology and Microbiology Section; anti-arthritis; anti-inflammatory cytokine