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DNaseⅠ在多发性肌炎和皮肌炎中的作用 被引量:2

Contribution of DNaseⅠin patients with polymyositis and dermatomyositis
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摘要 目的研究DNaseⅠ在多发性肌炎和皮肌炎发病机制中的作用。方法选择2011年12月至2012年10月在中日友好医院风湿免疫科住院患者中符合多发性肌炎(PM)/皮肌炎(DM)诊断标准的61例患者作为病例组。同期选择48例健康成年人作为对照组。辐射状酶扩散法测定血浆Ⅰ型脱氧核糖核酸酶(DNaseⅠ)活性,并与患者血清学指标进行相关性分析。在DNaseⅠ活性受损的患者血浆中添加外源性DNaseⅠ和微球菌核酸酶(MNase),进一步分析DNaseⅠ活性受损的原因。结果 DNaseⅠ活性在PM/DM组为(0.3353±0.1894)U/ml,显著低于健康对照组[(0.5441±0.2536)U/ml,P<0.0001]。36例DNaseⅠ活性显著受损的患者血浆中添加外源性重组DNaseⅠ后,11例患者的血浆不能明显恢复DNaseⅠ活性,而添加MNase后,患者血浆对底物dsDNA的降解完全恢复,说明这些患者血浆中存在DNaseⅠ的特异性抑制剂。相关性分析提示DNaseⅠ活性与血清球蛋白(r=0.366,P=0.005)和IgG(r=0.322,P=0.012)呈正相关。结论 PM/DM患者血浆DNaseⅠ活性显著低于健康对照;部分PM/DM患者血浆中存在DNaseⅠ的特异性抑制剂;DNaseⅠ的活性受损可能在PM/DM发病中起一定作用。 Objective To investigate activity of plasma DNaseⅠin patients with polymyositis ( PM ) and dermatomyositis ( DM ) .Methods From the Department of Rheumatology of China-Japan Friendship Hospital ( December 2011 to October 2012 ) ,61 patients who satisfied the Bohan &amp; Peter criteria for PM/DM were recruited for this study.To form a control group,48 age and sex-matched healthy Chinese adults were selected during the same period.DNaseⅠactivity was measured by radial enzyme-diffusion method.The mechanism of impaired DNaseⅠactivity was further analyzed by adding exogenous DNaseⅠand MNase to plasma samples .Correlation analysis were performed between DNase I activity and other serological items .Results DNaseⅠactivity in PM/DM group was (0.3353 ±0.1894 ) U/ml,significantly lower than that in healthy control group [(0.5441 ±0.2536 ) U/ml,P 〈0.0001 ] .Eleven patients with PM/DM cannot completely restore DNaseⅠactivity by adding exogenous DNaseⅠbut restore DNaseⅠactivity after being added MNase , indicating specific inhibitor of DNaseⅠoccurring in plasma of these patients .DNaseⅠactivity positively correlated with globulin ( r=0.366 , P=0.005 ) and IgG ( r=0.322 , P=0.012).Conclusion DNaseⅠactivity is impaired in PM/DM patients.Specific inhibitors of DNaseⅠoccur in plasma of a subset of PM/DM patients.Impaired DNaseⅠactivity may play a role in pathogenesis of PM/DM.
出处 《中华临床医师杂志(电子版)》 CAS 2013年第13期78-80,共3页 Chinese Journal of Clinicians(Electronic Edition)
关键词 多发性肌炎 皮肌炎 脱氧核糖核酸酶Ⅰ Polymyositis Dermatomyositis Deoxyribonuclease Ⅰ
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参考文献19

  • 1Dalakas MC,Hohlfeld R. Polymyositis and dermatomyositis[J].The Lancet,2003.971-982.
  • 2Dalakas MC. Polymyositis.dermatomyositis and inclusion-body myosi-tis[J].New England Journal of Medicine,1991.1487-1498.
  • 3Dalakas MC. Pathogenesis and therapies of immune-mediated myopa-thies[J].Autoimmunity Reviews,2012.203-206.
  • 4Denny MF,Chandaroy P,Killen PD. Accelerated macrophage apoptosis induces autoantibody formation and organ damage in system-ic lupus erythematosus[J].Journal of Immunology,2006.2095-2104.
  • 5Kaplan MJ. Apoptosis in systemic lupus erythematosus[J].Clinical Immunology,2004.210-218.
  • 6Brinkmann V,Reichard U,Goosmann C. Neutrophil extracellular traps kill bacteria[J].Science,2004.1532-1535.
  • 7Fuchs TA,Abed U,Goosmann C. Novel cell death program leads to neutrophil extracellular traps[J].Journal of Cell Biology,2007.231-241.
  • 8Chitrabamrung S,Rubin RL,Tan EM. Serum deoxyribonucleaseⅠand clinical activity in systemic lupus erythematosus[J].Rheumatology International,1981.55-60.
  • 9Valle FM,Balada E,Ordi-Ros J. DNase 1 and systemic lupus er-ythematosus[J].Autoimmunity Reviews,2008.359-363.
  • 10Lande R,Ganguly D,Facchinetti V. Neutrophils activate plasma-cytoid dendritic cells by releasing self-DNA-peptide complexes in sys-temic lupus erythematosus[J].Sci Transl Med,2011.73ra19.

同被引文献37

  • 1Zong M, Lundberg IE. Pathogenesis, classification and treatment of inflammatory myopathies. Nat Rev Rheumatol, 2011, 7: 297- 306.
  • 2Dalakas MC. Pathogenesis and therapies of immune-mediated myopathies. Autoimmun Rev, 2012, 11: 203-206.
  • 3Danoff SK, Casciola-Rosen L. The lung as a possible target for the immune reaction in myositis. Arthritis Res Ther , 2011, 13: 230.
  • 4Hirakata M, Nagai S. Interstitial lung disease in polymyositis and dermatomyositis. CUIT Opin Rheumatol, 2000, 12: 501-508.
  • 5Cheng OZ, Palaniyar N. NET balancing: a problem in inflam?matory lung diseases. Front Immunol, 2013, 4: 1.
  • 6Brinkmann V, Reichard U, Goosmann C, et al. Neutrophil extracellular traps kill bacteria. Science, 2004, 303: 1532-1535.
  • 7Fuchs TA, Abed U, Goosmann C, et al. Novel cell death program leads to neutrophil extracellular traps.J Cell Bioi, 2007, 176: 231-241.
  • 8Khandpur R, Carmona-Rivera C, Vivekanandan-Giri A, et al. NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis. Sci Transl Med, 2013, 5: 178ra40.
  • 9Keshari RS, Iyoti A, Dubey M, et al. Cytokines induced neutro?phil extracellular traps formation: implication for the inflamma?tory disease condition. PLoS ONE, 2012, 7: e48111.
  • 10Downey DG, Bell SC, ElbomJS. Neutrophils in cystic fibrosis. Thorax, 2009, 64: 81-88.

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