A Pilot Study on the Anti-Inflammatory Effects of Tacrolimus in Ankylosing Spondylitis: Evidence from Human Samples and a Murine Model
Sooin Park1,†
, Moon-Ju Kim1,†, Yu Jeong Lee1,2, Sung Min Yu1,2, Hae-in Lee3, So-Hee Jin1, A-ra Choi1,4, Seung Cheol Shim5, Eun Jeong Won6, Tae-Jong Kim1,2
1Department of Rheumatology, Chonnam National University Medical School, Gwangju, Republic of Korea
2Department of Biomedical Sciences, Graduate School of Chonnam National University, Gwangju, Republic of Korea
3Division of Biodurg Evaluation, NDDC, Osong Medical Innovation Foundation (KBIOHealth), Cheongju, Republic of Korea
4College of Nursing, Nambu University, Gwangju, Republic of Korea
5Division of Rheumatology, Daejeon Rheumatoid and Degenerative Arthritis Center, Chungnam National University Hospital, Daejeon, Republic of Korea
6Department of Laboratory Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea
Keywords: Ankylosing spondylitis, anti-inflammatory effects, tacrolimus
Abstract
Background/Aims: This study aimed to evaluate the potential anti-inflammatory and therapeutic effects of tacrolimus in ankylosing spondylitis (AS).
Materials and Methods: Peripheral blood mononuclear cells (PBMCs) and synovial fluid mononuclear cells (SFMCs) from AS patients were treated with tacrolimus and analyzed via flow cytometry to measure inflammatory cytokine-producing cells (IFN-γ, IL-17A, and GM-CSF). Additionally, cytokine levels (IFN-γ, IL-17A, TNF-α, and GM-CSF) in ex vivo cultured PBMC supernatants were quantified using enzyme-linked immunosorbent assay (ELISA). The in vivo effects of tacrolimus were assessed in an AS mouse model by evaluating clinical arthritis scores and analyzing inflammatory cytokine-producing cells (IFN-γ, IL-17A, and TNF-α) via flow cytometry.
Results: Tacrolimus significantly suppressed the production of inflammatory cytokines (IFN-γ, IL-17A, and GM-CSF) in PBMCs and SFMCs from AS patients. Cytokine levels (IFN-γ, IL-17A, TNF-α, and GM-CSF) in ex vivo PBMC cultures were also markedly reduced with tacrolimus treatment. In the AS mouse model, tacrolimus treatment resulted in significantly lower clinical arthritis scores and reduced production of inflammatory cytokines (IFN-γ, IL-17A, and TNF-α).
Conclusion: Tacrolimus demonstrates potential as a therapeutic agent for AS by suppressing inflammatory cytokine production in PBMCs and SFMCs from AS patients and exhibiting anti-inflammatory effects in an arthritis mouse model.
† These authors have contributed equally to this work and share first authorship.
Cite this article as: Park S, Kim M, Jeong Lee Y, et al. A pilot study on the anti-inflammatory effects of tacrolimus in ankylosing spondylitis: evidence from human samples and a murine model. ArchRheumatol. 2025;40(2):189-196.