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

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

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.

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.

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.