Oxidative DNA and mitochondrial DNA change in patients with SLE

Hui Ting Lee, Tsai Hung Wu, Chen Sung Lin, Chyou Shen Lee, Siao Cian Pan, Deh Ming Chang, Yau Huei Wei, Chang Youh Tsai*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

16 Scopus citations


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-γ 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.

Original languageEnglish
Pages (from-to)493-503
Number of pages11
JournalFrontiers in Bioscience - Landmark
Issue number3
StatePublished - 01 01 2017
Externally publishedYes


  • Chemokine
  • Interferon
  • Mitochondrial DNA
  • Oxidative stress
  • Systemic lupus erythematosus; interleukin


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