[Study on experimental systemic lupus erythematosus mouse model induced by pristane].

Aim: To establish the systemic lupus erythematosus (SLE) mouse model through pristane intraperitoneal injection and discuss the pathogenesis of SLE in this mouse model.

Methods: Single intraperitoneal injection of 0.5 mL Pristane or PBS was applied on 6-8 week old female BALB/c mice. The percentage of IFN-α producing cells (CD11b(+);Ly6C(high);)and B cells and the expression of B cell activation surface marker(Aβ1(d);)in peripheral blood were detected by flow cytometry every 2 weeks. Serum total IgG and auto-antibodies (anti-dsDNA, anti-sm RNP, anti-ribosomal P0)were detected by ELISA at different time point. The percentage of peritoneal CD11b(+);Ly6C(high);cells and Aβ1(d);expression in spleen were also detected by flow cytometry after 6 months. glomerular IgG deposition and kidney histopathologic changes were determined by direct immunofluorescence and H&E staining respectively.

Results: Total IgG began to increase since 2 months after the pristane injection, while auto-antibodies were detected after 3 moths, both of which peaked after 6 moths and maintained the high level. Most of the pristane treated mice developed arthritis, glomerular immune complex deposition and kidney damage. The percentage of peripheral and peritoneal IFN-α producing cells was much higher in pristane group than that of the PBS control group since 2 weeks after intraperitoneal injection. The mean fluorescence intensity (MFI) of B cell activation marker(Aβ1(d);) in pristane group was also higher than PBS group in both peripheral blood and spleen indicating B cell over activation.

Conclusion: Intraperitoneal injection of pristane can successfully establish a SLE mouse model which may be used in research of the SLE pathogenesis. Increased percentage of IFN-αproducing cells may play an etiopathogenic role in abnormal B cell activation and SLE development in this model.