Highlights
- •Both IL-10 and miR-96 were overexpressed during remission compared with relapse.
- •No correlation was found miR-96 expression and IL-10 levels during relapse or remission phases of MS.
- •miR-96 contributes to the remission in MS but not via IL-10 pathway.
Abstract
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.
Keywords
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Article info
Publication history
Published online: June 18, 2019
Received in revised form:
May 27,
2019
Received:
January 27,
2019
Identification
Copyright
© 2019 Elsevier B.V. All rights reserved.
