Abstract: Objective To observe the role and mechanism of IL-10 in the acute phase of Schistosoma japonicum infection in model mice infected by Schistosoma japonicum for new theoretical basis in prevention and treatment of liver fibrosis. Methods Abdominal patch was used to develop mouse models. After two days of infection with Schistosoma japonicum, IL-10R blocking antibody was intraperitoneally applied to the infected mice in experimental group once every two weeks, and Rat IgG1 was administered in mice in control group in the same protocol. By the 6th week, the serum and liver samples were taken to measure the indicators involved in liver fibrosis, including serum ALT level, and pathological changes of the liver after staining with H&E and Sirius red. Flow cytometry was used detect changes of macrophage subgroups in liver tissues,and quantitative PCR, ELISA and CBA were performed to detect the variation of liver inflammatory factors. Results Elevated ALT level( t= 5. 505,P<0. 05), enlarged granuloma in individual egg( t= 4. 817,P<0. 05), increased collagen deposition and count of pro-inflammatory Ly6C^hi acrophages in the liver( t= 27. 63,P<0. 05) as well as boosted local inflammatory factors, including CCL2, CCL3, CCL4, CCL5, TNF-α, IL-1b、IL-6、IL-12a and IL-12b, were seen in mice in the experimental group infected with Schistosoma japonicum compared to those in the control group. Conclusion Aggravated inflammation and fibrosis phenotype seen in mice with Schistosoma japonicum infection following IL-10R blocking antibody treatment proves that IL-10 plays an extremely important role in regulating the liver inflammation and fibrosis caused by Schistosoma japonicum, and our findings can provide a new consideration in treating schistosomiasis using IL-10 as the target.

Key words: Schistosoma japonicum, IL-10, Inflammatory factors, Chemokine, Liver fibrosis