Application of tuberculous bacterium H37Ra in the experimental autoimmune myasthenia gravis model with rat acetylcholine receptor alpha subunit 97-116 peptide as immunogen
JING Feng CHEN Bing
Department of Neurology, the 8th Medical Center of Chinese PLA General Hospital, Beijing 100091, China
Abstract：Objective To investigate the role of mycobacterium tuberculosis H37Ra in the establishment of myasthenia gravis animal models with rat acetylcholine receptor alpha subunit 97-116 peptide (R97-116) as an immunogen.Methods Subcutaneous inoculation was carried out in the foot pad and skin of Lewis rats with R97-116 as the immunogen. Twenty rats were divided into the experimental group and control group according to whether H37Ra was added, and a blank control group was set up at the same time. The difference of behavior, body weight and antibody titers of acetylcholine receptors between the three groups was compared.Results In the experimental group, local inflammation was obvious,three rats died, six showed asthenia and positive antibodies, and one showed no obvious abnormal manifestations. In the control group, local inflammatory reactions were also present, and only two showed symptoms of mild weakness, one of which was suspected of having positive antibodies and the other one was negative. The weight of the experimental group [(190.21±8.35)g] was significantly lower than that of the control group [(243. 22±7.98)g] and the blank control group[(251.22±5.81)g], and the difference was statistically significant (P<0.05), but there was no statistically significant difference between the control group and the blank control group.Conclusion H37Ra is a necessary reagent for the success of this experiment.
Shan W, Li H, Min Z, et al. Curcumin ameliorates experimental autoimmune myasthenia gravis by diverse immune cells[J]. Neurosci Lett, 2016,626:25-34.
[3]
Verma R, Pinto S M, Patil A H, et al. Quantitative Proteomic and phosphoproteomic analysis of H37Ra and H37Rv strains of mycobacterium tuberculosis[J]. J Proteome Res, 2017,16(4):1632-1645.
[4]
Baggi F, Annoni A, Ubiali F, et al. Breakdown of tolerance to a self-peptide of acetylcholine receptor alpha-subunit induces experimental myasthenia gravis in rats[J]. J Immunol, 2004,172(4):2697-2703.
[5]
Lennon V A, Lindstrom J M, Seybold M E. Experimental autoimmune myasthenia: a model of myasthenia gravis in rats and guinea pigs[J]. J Exp Med, 1975,141(6):1365-1375.
[6]
Patrick J, Lindstrom J. Autoimmune response to acetylcholine receptor[J]. Science, 1973,180(4088):871-872.
[7]
Zhang Y, Frutiger S, Hughes G J, et al. Identification of T-cell epitopes of autoantigens using recombinant proteins; studies on experimental autoimmune myasthenia gravis[J]. Immunology, 1990,71(4):538-543.
[8]
Wang C C, Zhang M, Li H, et al. Caspase-1 inhibitor regulates humoral responses in experimental autoimmune myasthenia gravis via IL-6- dependent inhibiton of STAT3[J]. Neurosci Lett, 2017,656:169-176.
[9]
Gooch J W. Antigenic Determinant[M]. NewYork: Springer, 2011: 874-874.
[10]
Lazaridis K, Baltatzidi V, Trakas N, et al. Characterization of a reproducible rat EAMG model induced with various human acetylcholine receptor domains[J]. J Neuroimmunol, 2017,303:13-21.
[11]
Boradia V M, Patil P, Agnihotri A, et al. Mycobacterium tuberculosis H37Ra: a surrogate for the expression of conserved, multimeric proteins of M.tb H37Rv[J]. Microb Cell Fact, 2016,15(1):140-157.
2019, Vol. 30 
