Objective: It has been suggested that C-C motif chemokine ligand 20 (CCL20) is an important inflammatory mediator and a central regulatory molecule in liver fibrosis. Recent reports indicate a potential role for visfatin, an adipocytokine, in hepatic inflammation and fibrosis. Here, we investigated the CCL20 expression by visfatin and its signaling pathways in human macrophage cell line, THP-1 cells. Methods: After treatment with visfatin, CCL20 expression and production was analyzed by RT-PCR and ELISA in THP-1 cells. We also assessed the intracellular signaling molecules including NF-κB, IKK, p38 and JNK using immunoblotting analysis. We treated THP-1 cells with visfatin or visfatin along with SP600125 (a JNK inhibitor), SB203580 (a p38 inhibitor), or Bay 7082 (a NF-κB inhibitor) for 24h, then evaluated CCL20 mRNA using RT-PCR and signaling pathways using immunoblotting. To investigate the effects of visfatin-induced CCL20 on hepatic stellate cells, THP-1 cells treated with visfatin were co-cultured with LX-2 human hepatic stellate cells, and fibrosis markers were examined by RT-PCR and immunoblotting. Results: Visfatin enhanced CCL20 mRNA expression and production in THP-1 cells. Visfatin also increased intracellular signaling molecules such as NF-κB, IKK, p38 and JNK. Visfatin treatment along with JNK, p38 or NF-κB inhibitors significantly reduced CCL20 expression. After LX-2 cells were cultured with the supernatant of visfatin-treated THP-1 cells, mRNA expressions of TIMP1, collagen 1, MMP2, α-SMA and CCR6 were increased in LX-2 cells; together with CCL20 neutralization antibody, mRNA expressions of fibrosis markers were reduced. Conclusion: Visfatin increased CCL20 production in macrophages via p38 and JNK signaling pathways, and visfatin-induced CCL20 contributed to the activation of hepatic stellate cells.