GUT MICROBIOTA AND PAIN EXPRESSION IN ANKYLOSING SPONDYLITIS: CLINICAL-MICROBIAL CORRELATES (GRASP-STUDY)

L. Chislari¹, A. Lobiuc², E. Russu³, M. Homitchi⁴, C. Ciorescu¹, N. Paval², M. Covasa², L. Groppa¹ | ¹Nicolae Testemitanu State University of Medicine and Pharmacy, Chisinau, Republic of Moldova; ²Faculty of Medicine and Biological Sciences, Stefan cel Mare State University of Suceava, Romania; ³Nicolae Testemitanu State Medical and Pharmaceutical University; Timofei Mosneaga Republican Clinical Hospital, Chisinau, Republic of Moldova; ⁴Timofei Mosneaga Republican Clinical Hospital, Chisinau, Republic of Moldova

Abstract

Background and Aims. Pain is the dominant clinical manifestation in ankylosing spondylitis (AS), reflecting both structural inflammation and neuroimmune mechanisms. Emerging evidence suggests that gut microbiota dysbiosis may contribute to systemic inflammation and pain amplification. This study aimed to evaluate the relationship between intestinal microbiota composition and pain expression in AS.
Methods. A cohort of 60 subjects (41 AS patients, 19 controls) was analyzed. Patients were stratified into axial (axAS) and peripheral (pAS) phenotypes. Clinical data included inflammatory markers and disease activity indices. Pain intensity was assessed indirectly through disease activity parameters. Gut microbiota composition was evaluated using PCR-based analysis, followed by multivariate and classification modeling.
Results. AS patients demonstrated a distinct microbial profile compared to controls (p < 0.001), with 12 predominant bacterial species identified versus 8 in controls. A significant reduction in Bacteroides (0.332 vs. 0.430) and marked increase in Prevotella (0.168 vs. 0.031) were observed, indicating dysbiosis associated with inflammatory activation. Patients with peripheral AS exhibited earlier disease onset (18.0 vs 25.5 years; p < 0.01) and higher inflammatory burden, corresponding to increased pain-related clinical expression. Multivariate analysis identified 8 microbial genera (including Dialister, Collinsella, and Streptococcus) as key discriminators of AS, with a classification accuracy of 95%, suggesting strong biological relevance. These taxa are known to induce pro-inflammatory pathways, supporting a mechanistic link between gut dysbiosis and nociceptive sensitization.
Conclusions. Gut microbiota alterations are associated with inflammatory activity and pain expression in AS. Microbial profiling may represent a novel biomarker for early identification of high-pain phenotypes and a potential therapeutic target.