ObjectiveTo determine whether the observed increased expression of the proinflammatory cytokine interleukin (IL)-17 in fibrotic liver tissues functions to promote fibrosis by mediating the activation of heptatic stellate cells (HSCs) and modulating their expression of fibrosis-related factors, such as alpha-smooth muscle actin (α-SMA), collagen I, collagen III, and fibronectin. MethodsA murine model system of liver fibrosis was established by injecting male C57BL/6J mice (6-8 weeks old) with CCl4 (1.5 μl/g of 1∶6 dilution in olive oil) twice weekly for eight weeks; control mice were similarly injected with olive oil alone. Human liver tissue samples were collected from 32 patients with liver fibrosis (including 19 cases of chronic hepatitis B, three cases of autoimmune hepatitis, six cases of alcoholic liver disease, and four cases of primary biliary cirrhosis) and three healthy controls. The rat HSC-T6 cell line was cultured under standard conditions (controls) or treated with 100 nM of IL-17 for 6 h. Differential expression of IL-17, α-SMA, collagen I, collagen III, and fibronectin mRNA and protein was detected by the real-time fluorescent quantitative PCR or immunohistochemical staining, respectively. Significance of intergroup diffrences was assessed by Student’s t-test, and correlation of differences with fibrosis was assessed by calculating the linear correlation coefficient. ResultsThe fibrotic liver tissues from both the mouse model and human patients showed significantly higher IL-17 expression than the non-fibrotic control tissues (mouse mRNA: t=4.84, P＜0.01; human protein: t=2.82, P＜0.01). IL-17 treatment of HSC-T6 cells led to significantly increased mRNA expression of α-SMA, collagen I, collagen III, and fibronectin (all P＜0.05). In the human liver tissues, IL-17 protein expression was found to be positively correlated with increased α-SMA protein expression (r=0.78). ConclusionEnhanced IL-17 in fibrotic liver tissues may act to promote expression of α-SMA, collagen I, collagen III, and fibronectin in HSCs, thereby contributing to the development of liver fibrosis.