Therapeutic efficacy of Bacillus clausii via NFκB/Nrf-2/HO-1 pathway modulation in a CFA-induced arthritis model

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by dysregulated cytokine signalling, oxidative stress, and persistent synovial inflammation. Nearly 0.24-1 % of people worldwide suffer from RA, caused by complex genetic and environmental factors leading to joint destruction and inflammation cascades.

Using a complete Freund's adjuvant (CFA)-induced murine model of arthritis, this study investigated the immunomodulatory and antioxidant properties of Bacillus clausii (1 × 10⁸ CFU/animal/day, orally) administered as a pre-treatment, concurrent, and adjunct intervention over 28 days.

It was evident from histological and radiological investigations that B. clausii considerably reduced joint damage, arthritic index scores, and paw swelling. Better nociceptive and affective results from behavioural tests suggested anti-nociceptive and anti-depressive effects. Furthermore, B. clausii altered critical inflammatory pathways and considerably decreased oxidative stress by upregulating HO-1 and Nrf-2; these effects were confirmed by downregulating IFN-γ, IL-17, IL-6, and phosphorylated NF-κB.

These findings suggest that B. clausii has a variety of therapeutic effects in RA by targeting oxidative and inflammatory mediators without producing long-term toxicity. Due to its favourable safety and efficacy profile, it may be a valuable adjunct to conventional anti-arthritic treatments.