Oxidative DNA and mitochondrial DNA change in patients with SLE.

We evaluated plasma IL-10, IFN-alpha, IL-23, IFN-gamma, IP-10, MCP-1, 8-OHdG, leukocyte mtDNA, serum anti-dsDNA antibodies and disease activity index (SLEDAI) in SLE patients. 93 patients (35 nephritis, 4 under dialysis, 5 under rituximab) and 50 healthy controls were recruited. Compared with healthy controls, SLE patients had higher IL-10, IFN-alpha, IL-23, IFN-gamma, IP-10 and MCP-1 ( p <0.05). High IFN-alpha ( p =0.031) and IP-10 ( p =0.026) correlated with high SLEDAI; high IFN-alpha ( p< 0.001), IL-23 ( p =0.023) and IP-10 ( p< 0.001) correlated with high anti-dsDNA. High IL-10 ( p =0.014), IL-23 ( p< 0.001), IFN-gamma ( p< 0.001) and MCP-1 ( p =0.002) correlated with high 8-OHdG and high IL-23 ( p <0.001), INF-gamma ( p <0.001), IP-10 ( p =0.023) and MCP-1 ( p =0.002) correlated with low leukocyte mtDNA. mtDNA 4977 deletion correlated with high mtDNA ( p =0.011) and low IL-10 ( p =0.009). MCP-1 ( p =0.043) decreased after rituximab therapy. 54 SLE patients without nephritis, 35 with nephritis but without dialysis, and 4 with nephritis under dialysis exhibited stepwise increases in IL-23 ( p =0.009) and MCP-1 ( p =0.015). These data suggest that oxidative DNA and mtDNA alterations and coordinate changes in cytokines/chemokines are implicated in progression of SLE and rituximab in amelioration of SLE.