Differential Expression of Visfatin, Sirtuin-1, and Interleukin-18 in Ankylosing Spondylitis Patients: A Comparative Study of Etanercept-Treated versus Newly Diagnosed Patients.

Authors

Afrouz Asgarian, Zahra Hesari, Mehrdad Aghaei, Zahra Faghhian, Romina Malakouti, Sima Besharat, Koushan Sineh Sepehr

Published in

Iranian journal of medical sciences. Volume 51. Issue 8. Pages 554-560. Epub Aug 01, 2026.

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory disease primarily affecting the axial joints. In response to inflammation, sirtuin-1 (SIRT-1) plays a regulatory role by modulating inflammatory signaling pathways and protecting against further tissue damage. Interleukin-18 (IL-18) is a potent pro-inflammatory cytokine released predominantly by pyroptotic immune cells. Visfatin, an adipokine secreted by lymphocytes and other immune cells, is increasingly recognized as a pro-inflammatory mediator implicated in various rheumatologic disorders. This study aimed to evaluate the expression levels of SIRT-1, IL-18, and visfatin genes in immune cells of AS patients.
In 2022, this cross-sectional study was conducted in Gorgan, Iran. Peripheral blood mononuclear cells (PBMCs) were isolated from a total of 49 AS patients, including patients undergoing treatment with three doses of etanercept and the newly diagnosed, treatment-naïve patients. Total RNA was extracted from PBMCs, and complementary DNA (cDNA) was synthesized. Gene expression levels of SIRT-1, IL-18, and visfatin were quantified using real-time PCR, and data were analyzed using SPSS v16 and GraphPad Prism 9 with Student's t test. A significant difference was considered as P<0.05.
SIRT-1 expression was significantly lower in newly diagnosed AS patients than in the etanercept-treated group (P=0.041). Visfatin expression was significantly higher in the new case group than in the treated group (P=0.021). Similarly, IL-18 expression was significantly higher in new cases than in etanercept-treated patients (P=0.028).
Etanercept significantly upregulates SIRT-1 expression while suppressing IL-18 and visfatin levels in AS patients, highlighting its pleiotropic anti-inflammatory mechanisms beyond TNF-α blockade. These findings provide novel insights into the molecular pathways modulated by anti-TNF therapy, particularly the interplay between SIRT1-mediated epigenetic regulation and adipokine-driven inflammation.

PMID:
42764882
Bibliographic data and abstract were imported from PubMed on 21 Sep 2026.

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