Expression levels of miR-146a and miR-155 and their association with Interleukin-6 in type 1 diabetes
- Authors: Natiq Z.A.1, Nader M.I.1
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Affiliations:
- Institute of Genetic Engineering and Biotechnology for Postgraduate Studies, University of Baghdad
- Issue: Vol 15, No 6 (2025)
- Pages: 1130-1136
- Section: ORIGINAL ARTICLES
- URL: https://journals.rcsi.science/2220-7619/article/view/380247
- DOI: https://doi.org/10.15789/2220-7619-ELO-17984
- ID: 380247
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Full Text
Abstract
Background. Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disease characterized by the immune-mediated destruction of pancreatic beta cells, leading to insulin deficiency. Inflammatory cytokines, particularly interleukin-6 (IL-6), play a central role in this pathological process by promoting pro-inflammatory immune responses. Recent evidence highlights the involvement of microRNAs, especially miR-146a and miR-155, in regulating immune cell activation and cytokine signaling pathways. Dysregulation of these microRNAs may disrupt immune homeostasis and contribute to the progression of T1DM. This study aimed to investigate the expression levels of miR-146a and miR-155 in patients with T1DM and to examine their association with serum IL-6 concentrations. Materials and methods. This case-control study included 150 participants, comprising 100 individuals diagnosed with T1DM and 50 healthy controls. Peripheral blood samples were collected to evaluate fasting blood glucose, glycated hemoglobin, and IL-6 levels using an enzyme-linked immunosorbent assay. Quantitative real-time polymerase chain reaction was used to assess the expression of miR-146a and miR-155, normalized to miR-16 as the internal control. Results. The results revealed significantly elevated levels of fasting blood glucose, glycated hemoglobin, and IL-6 in patients compared to controls (p < 0.0001). Additionally, miR-146a expression was increased by a 3.1-fold change, and miR-155 showed a 1.58-fold increase in patients with T1DM compared to healthy individuals. Conclusions. The significant overexpression of microRNAs miR-146a and miR-155, in parallel with elevated serum levels of the pro-inflammatory cytokine IL-6, highlights their crucial role in the immunopathogenesis of T1DM. These findings suggest that miR-146a and miR-155 may act as key regulators in modulating immune responses, contributing to the autoimmune destruction of pancreatic beta cells. Moreover, the combined assessment of these microRNAs and IL-6 may serve as valuable molecular biomarkers for early diagnosis, disease prognosis, and the development of novel immunomodulatory therapeutic strategies in T1DM management.
About the authors
Zahraa Abdullah Natiq
Institute of Genetic Engineering and Biotechnology for Postgraduate Studies, University of Baghdad
Author for correspondence.
Email: Zahraa.abd2300m@ige.uobaghdad.edu.iq
MSc of Genetic Engineering and Biotechnology
Iraq, BaghdadM. I. Nader
Institute of Genetic Engineering and Biotechnology for Postgraduate Studies, University of Baghdad
Email: Zahraa.abd2300m@ige.uobaghdad.edu.iq
PhD
Iraq, BaghdadReferences
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