Two chemokine biomarkers displayed significantly reduced levels in patients with systemic lupus erythematosus who were treated when compared with untreated patients, according to recent study results.
Researchers collected blood from 103 patients with systemic lupus erythematosus (SLE) and 65 healthy donors who were enrolled from 2008 to 2011 in the University of Florida Center for Autoimmune Diseases registry. Taqman real time polymerase chain reaction assays were used to isolate and analyze RNA samples from peripheral blood leukocytes for expression of mRNA and micro RNA. The delta delta C(T) method was used to determine relative expression of interferon signature genes, C-C motif chemokine ligand 2 (CCL2) and C-X-C motif chemokine 10 (CXCL10).
“Results were correlated with therapy using prednisone, mycophenolate mofetil and hydroxychloroquine and analyzed by Wilcoxon/Kruskal-Wallis test and Fisher’s exact test,” the researchers wrote.
Untreated patients had significantly greater levels of CCL2 and CXCL10 compared with treated patients. Treated and untreated patient visits showed no significant difference in high signal transducers and activators of transcription (STAT)1. Untreated patients and those with high STAT1 had significantly higher slopes of linear regression fits of interferon (IFN) score compared with treated patients.
Differences between the slopes of high STAT1 and untreated patients were not significant, which indicated that CCL2 and CXCL10 were correlated with type-1 IFN in high STAT1 patients and similar to untreated patients.
During treated patient visits, CCL2 and CXCL10 levels remained elevated in the high STAT1 subset compared with those in the low STAT1 subset.
“We consider reduction of CCL2 and CXCL10 as good indicators of successful therapy, while elevation in STAT1 levels may indicate therapy resistance,” the researchers concluded. “Further work is needed to determine the role that STAT1 plays in therapy. Our study raises an interesting question whether SLE patients with high STAT1 status can benefit from therapy with specific STAT1 inhibitors.”
Disclosure: The researchers report no relevant financial disclosures.