Abstract
Objective. To investigate the relationship between NLRP3 and the pathogenesis of collagen-induced arthritis. Methods. We used the collagen-induced arthritis (CIA) mouse model. The mice were divided into two groups: the model group (CIA, n = 16) and the control group (Normal, n = 8). The mice were sacrificed seven weeks after immunization. The arthritis score and imaging evaluation (X-rays, Micro-CT, and MRI) were performed. Synovial tissue NLRP3 expression and peripheral blood cytokine levels were analyzed. Results. The arthritis score (6.00 ± 2.52), imaging score (4.63 ± 0.92), and synovial tissue NLRP3 expression (4.00 ± 2.03) significantly increased in the CIA mice. The expression of synovial NLRP3 was positively correlated with arthritis clinical and radiographic scores (r = 0.792 and r = 0.669, resp.). Conclusions. The synovial NLRP3 expression increased at the early onset of RA. Synovial NLRP3 expression level was correlated with the clinical arthritis severity and extent of radiological destruction, suggesting that NLRP3 is involved in the pathogenesis of RA.
Highlights
Rheumatoid arthritis (RA) is a systemic chronic and progressive autoimmune disease
Studies on gout pathogenesis have demonstrated that a single crystal of sodium urate can change NLRP3 configuration, resulting in NLRP3 activation and release of a large number of proinflammatory cytokines, including IL-1β, which participate in the pathogenesis of arthritis [25]
Our study shows that serum IL1β, IL-18, and IL-33 in collagen-induced arthritis (CIA) mice significantly increased compared with Normal mice, which are consistent with previous findings
Summary
Rheumatoid arthritis (RA) is a systemic chronic and progressive autoimmune disease. The antagonists that target these factors, such as soluble IL-1 receptor, IL1 receptor antagonist, and IL-6 monoclonal antibodies, are widely used in the treatment of RA. The therapeutic methods that are targeting NLRP3 inflammasome, the upstream factors of IL-1 families, may provide a new means for the treatment of RA. Studies show that small molecule compounds MCC950 can reduce the severity of experimental autoimmune encephalomyelitis and multiple sclerosis in mice by blocking NLRP3 activation [3]. Understanding the relationship between NLRP3 and the pathogenesis of RA is a key point for deeper understanding of the “NLRP3 inflammasome signaling pathways” and the pathogenesis of RA and may provide new targets for the treatment of RA
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