Gut microbiota and ankylosing spondylitis: current insights and future challenges
Authors:Andrei Lobiuc1, Liliana Groppa2, Lia Chislari2, Eugeniu Russu2,3, Marinela Homitchi2,3, Camelia Ciorescu2,3, Sevag Hamamah4, I. Codruta Bran1 and Mihai Covasa1
1 Department of Biological and Morphofunctional Sciences, College of Medicine and Biological Science, Stefan cel Mare University of Suceava, 720229 Suceava, Romania. 2 Department of rheumatology and nephrology, Nicolae Testemițanu State University of Medicine and Pharmacy, Chișinău, Republic of Moldova. 3 Timofei Moșneaga Republican Clinical Hospital, Chișinău, Republic of Moldova. 4 Department of Internal Medicine, Scripps Mercy Hospital, San Diego, CA 92103, USA.
Keywords:
spondyloarthritis, dysbiosis, HLA-B27, autoimmune disease, gut-joint axis, IL-23/17 axis, microorganisms.
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Conflict of interest statement:
The authors declare that there is no conflict of interest concerning the publication of this manuscript.
Please cite this article as:
Andrei Lobiuc, Liliana Groppa, Lia Chislari,Eugeniu Russu, Marinela Homitchi, Camelia Ciorescu, Sevag Hamamah, I. Codruta Bran and Mihai Covasa (2025). Gut microbiota and ankylosing spondylitis: current insights and future challenges. Microbial Cell 12: 210-230. doi: 10.15698/mic2025.08.857
© 2025 Lobiuc et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
Ankylosing spondylitis (AS) is a chronic inflammatory disease with complex pathogenesis influenced by genetic, immunological and environmental factors. Recent evidence suggests that gut microbiota significantly contributes to AS etiopathogenesis. Dysbiosis and altered immune responses in the gut potentially trigger or exacerbate the disease through intestinal barrier disruption, alteration of the IL-23/17 axis and metabolite production. This review explores the growing role of gut microbiota in AS and its potential to reshape targeted treatment strategies and facilitate development of adjunct therapies to address disease onset and progression. AS is a multifactorial disease in which gut dysbiosis plays a significant role influencing immune regulation notably through the IL-23/17 pathway. Alterations in gut microbiota composition and its metabolites contribute to systemic inflammation, reinforcing a self-perpetuating feedback loop between gut and spinal inflammation that drives disease progression. Emerging evidence has linked microbial mechanisms to HLA-B27 misfolding promoting endoplasmic reticulum stress and triggering molecular mimicry through gut microbial-associated molecular patterns further contributing to AS pathogenesis. Given the crucial role of gut microbiota in AS, targeting microbiota imbalances presents a promising avenue for novel therapeutic strategies. Although it remains unclear whether gut inflammation and microbial changes precedes AS onset, current evidence suggests an ongoing cycle of autoimmune inflammation involving both the gut and joints. Further research, particularly longitudinal studies, are needed to better understand the gut-joint axis and its potential therapeutic implications in AS management.
doi: 10.15698/mic2025.08.857
Volume 12, pp. 210 to 230, published 25/08/2025.