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Background  The NF-κB signalling pathway has been reported to be related to liver fibrosis, and we investigated whether the NF-κB signalling pathway is involved in liver fibrosis caused by secreted phospholipase A2 of  Clonorchis sinensis  ( Cs sPLA2). Furthermore, expression of the receptor of  Cs sPLA2 on the cell surface of hepatic stellate cells (HSCs) may greatly contribute to liver fibrosis.    Methods   Cs sPLA2 was administered to BALB/c mice by abdominal injection. The levels of markers of NF-κB signalling pathway activation in mouse liver tissue were measured by quantitative RT-PCR, ELISA and western blot. Additionally, HSCs were incubated with  Cs sPLA2, and an NF-κB signalling inhibitor (BAY 11-7082) was applied to test whether the NF-κB signalling pathway plays a role in the effect of  Cs sPLA2. Then, the interaction between  Cs sPLA2 and its receptor transmembrane 7 superfamily member 3 (TM7SF3) was confirmed by co-immunoprecipitation (co-IP) and GST pull-down. To determine how TM7SF3 influences the ability of  Cs sPLA2 to cause liver fibrosis, a TM7SF3 antibody was used to block TM7SF3.    Results  The levels of the NF-ΚB signalling pathway activation markers TNF-α, IL-1β and phospho-p65 were increased by  Cs sPLA2 in the context of liver fibrosis. In addition, the interaction between TM7SF3 and  Cs sPLA2 was confirmed by co-IP and GST pull-down. When TM7SF3 was blocked by an antibody targeting 1–295 amino acids of TM7SF3, activation of HSCs caused by  Cs sPLA2 was alleviated.    Conclusions  The NF-ΚB signalling pathway is involved in the activation of HSCs by  Cs sPLA2. TM7SF3, the receptor of  Cs sPLA2, plays important roles in liver fibrosis caused by  Cs sPLA2.

The NF-κB signalling pathway and TM7SF3 contribute to liver fibrosis caused by secreted phospholipase A2 of Clonorchis sinensis