Interleukin 19 suppresses RANKL-induced osteoclastogenesis via the inhibition of NF-KB and p38MAPK activation and c-Fos expression in RAW264.7 cells

Interleukin 19 (IL-19) is a member of the IL-10 family of cytokines and is known as an inhibitory cytokine. IL-10, also an inhibitory cytokine, suppresses the receptor activator of nuclear factor KB (NF-KB) ligand (RANKL)induced osteoclast differentiation. However, the effects of IL-19 on osteoclast...

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Veröffentlicht in:Cytokine (Philadelphia, Pa.) Pa.), 2021-08, Vol.144, Article 155591
Hauptverfasser: Tsubaki, Masanobu, Takeda, Tomoya, Matsuda, Takuya, Yamamoto, Yuuta, Higashinaka, Aki, Yamamoto, Kasane, Tsurushima, Katsumasa, Ishizaka, Toshihiko, Nishida, Shozo
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Sprache:eng
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Zusammenfassung:Interleukin 19 (IL-19) is a member of the IL-10 family of cytokines and is known as an inhibitory cytokine. IL-10, also an inhibitory cytokine, suppresses the receptor activator of nuclear factor KB (NF-KB) ligand (RANKL)induced osteoclast differentiation. However, the effects of IL-19 on osteoclast differentiation are not currently well-understood. In this study, we examined whether IL-19 suppresses osteoclast differentiation in the mouse macrophage-like cell line RAW264.7. We found that IL-19 inhibited RANKL-induced osteoclast differentiation. In addition, IL-19 suppressed RANKL-induced NF-KB and p38 mitogen-activated protein kinase (p38MAPK) activation and c-Fos expression. Moreover, RANKL inhibited IL-19 mRNA expression and secretion in RAW264.7 cells, and the inhibition of the IL-19 function promoted osteoclast differentiation. These results indicate that IL19 suppressed osteoclast differentiation via the inhibition of NF-KB and p38MAPK activation and c-Fos expression. Furthermore, IL-19 may maintain the osteoclast precursor state, such as monocytes and macrophages. These findings may be useful in the development of osteoclast inhibitors, thereby improving treatments for osteoclast activation-related diseases, such as osteoporosis.
ISSN:1043-4666
1096-0023
DOI:10.1016/j.cyto.2021.155591