Abstract

Objective: Despite the clues that myasthenia gravis (MG) disease may be associated with inflammasomes, there are no studies in the literature on MG disease and inflammasome complexes. Hence, to address this question, we investigated the possible participation of inflammasomes in experimental autoimmune myasthenia gravis mouse model (EAMG). Material and Method: EAMG was induced in mouse using acetylcholine receptor (AChR) protein, and Anti-AChR IgG antibody levels detected by ELISA in the experimental group confirmed our model. Levels of CASP1, IL-1β, NLRP3, P2X7R, and AKT1 of the experimental and control (complete Freund’s adjuvant -CFA immunized) groups were measured by qRT-PCR. Results: After immunization, the AChR IgG antibody levels were significantly higher in the AChR-immunized group than in the control group (p=0.042). IL-1β levels in the experimental group were significantly higher, compared to the control group (p=0.01). CASP1, NLRP3, and P2X7R levels were also higher compared to the control group. However, these differences did not attain statistical significance (p>0.05). AKT1 levels were lower compared to the control group. There was no correlation between serum antibody concentration and gene expression levels. Conclusion: Our results suggest that there might be inflammasome involvement in the pathology of MG disease. Increase in IL-1β levels indicates the importance of the inflammatory response; however, further studies are necessary to confirm this.

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