Micro-RNA-96 and interleukin-10 are independent biomarkers for multiple sclerosis activity.

BACKGROUND: Micro-RNAs (miRNAs) are evolving as biological markers for multiple sclerosis (MS) both in activity and remission. miR-96 is associated with remission, however, the exact mechanism through which it contributes to the anti-inflammatory pathway is not clear. OBJECTIVE: To study the expression of miR-96 and IL-10 (anti-inflammatory mediator) in relapsing remitting (RR) MS. SUBJECTS AND METHODS: A case control study including 32 RRMS patients from Kasr Al-Ainy MS clinic, Cairo University, Egypt, and 26 healthy controls (HC). Assessment of serum IL-10 by ELISA, and miR-96 via real time PCR was done during relapse and remission in patients, and in HC. RESULTS: IL-10 was higher in RRMS patients during remission and in HC compared with relapse (P ˂ 0.001). miR-96 expression was higher in RRMS patients during remission compared with relapse and HC, and was higher in HC than in relapse (P ˂ 0.001). IL-10 level in remission correlated positively with disease duration (r = 0.41; P = 0.02). Otherwise, no correlation was found between IL-10 and relapse number or EDSS (P>0.05). miR-96 in relapse negatively correlated with EDSS in relapse (r=-0.47; P=0.007), but no correlation was found with disease duration or relapse number, whereas, miR-96 in remission did not correlate with any clinical parameters (P>0.05). No correlation was found between IL-10 and miR-96 either in relapse or remission (P>0.05). CONCLUSION: IL-10 and miR-96 are associated with MS quiescence, however, the lack of a significant correlation between them implicates that the influence of miR-96 may be exhibited through some pathway other than IL-10.

Role of interleukin-23 as a biomarker in rheumatoid arthritis patients and its correlation with disease activity.

BACKGROUND: IL-23 is a pro-inflammatory cytokine belonging to the IL-12 cytokine family. IL-23 is essential for the differentiation of Th17 lymphocytes, a subtype of T lymphocyte implicated in chronic inflammatory/autoimmune mediated diseases. Experimental models of arthritis and clinical indications have highlighted an important role for Th17 lymphocytes in the pathogenesis of RA. However the role and mechanism of action of IL-23 in the pathogenesis of RA are still not fully understood. OBJECTIVE: This study was conducted to assess the level of IL-23 in patients with RA as well as the relationship between the IL-23 level and disease activity. METHODS: The study includes 77 patients with RA fulfilling the American College of Rheumatology (ACR) revised criteria for diagnosis of RA as well as 25 age and sex matched healthy subjects as controls. Patients were divided according to disease activity into four groups: DAS 28 score (˂ 2.6), 10 patients in remission, DAS 28 score between 2.6-3.2, 10 patients with low disease activity, DAS 28 score ranges between (3.2-5.1), 30 patients with moderate disease activity and DAS 28 score (˂ 5.1), 27 patients with High disease activity. Disease activity were determined by the 28-joint disease activity score (DAS 28). Anti-citrullinated protein antibodies (ACPA) was done. The levels of IL-23 were determined by enzyme-linked immunosorbent assay (ELISA). RESULTS: Serum level of IL-23 was significantly elevated in RA patients (78.92±52.47) compared to control group (33.34±3.99) (P<0.001). However, no correlations were found between IL-23 and DAS 28 score, and other patients characteristics. CONCLUSION: Our results imply that IL-23 may potentially play a role in the pathogenesis of RA and may be a useful biomarker for the diagnosis of this disease. Targeting the IL-23 cytokine may provide a new therapeutic approach in the treatment of RA.