Decrease severity of collagen antibody and lipopolysacchride-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-32 beta 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-32 beta transgenic mice compared with non-transgenic mice. The populations of cytotoxic T, NK and dendritic cells was inhibited and NF-kappa B and STAT3 activities were significantly lowered in the CAIA and LPS-treated IL-32 beta transgenic mice. The expression of pro-inflammatory proteins was prevented in the paw tissues of CAIA and LPS-treated IL-32 beta transgenic mice. In addition, IL-32 beta altered several cytokine levels in the blood, spleen and paw joint. Our data indicates that IL-32 beta comprehensively inhibits the inflammation responses in the CAIA and LPS-induced inflammatory arthritis model.