脑梗死患者外周血调节性B细胞水平及其与颈动脉粥样硬化严重程度的相关性
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摘要
目的探讨脑梗死患者外周血调节性B细胞(Bregs)水平变化及其与颈动脉粥样硬化严重程度的相关性。方法选取2017-09-01—2018-05-01十堰市太和医院收治的动脉粥样硬化性脑梗死患者50例,并选择同期健康体检者50名为对照组。采用流式细胞术(FCM)检测外周血B细胞中CD19+CD5+CD1d+B细胞(Bregs)所占B细胞的比例;采用ELISA法测定Bregs培养液上清中白细胞介素-10(IL-10)及转化生长因子-β1(TGF-β1)水平。分析脑梗死患者外周血Bregs水平变化以及其与颈动脉粥样硬化程度的关系。结果脑梗死患者外周血Bregs水平及其分泌的IL-10、TGF-β1水平较对照组降低(P<0.05);随颈动脉粥样硬化严重程度加重,脑梗死患者外周血Bregs水平及IL-10、TGF-β1水平逐渐降低(均P<0.05)。结论动脉粥样硬化性脑梗死患者外周血Bregs水平低于健康人;Bregs水平与动脉粥样硬化性脑梗死患者颈动脉粥样硬化严重程度密切相关;外周血Bregs水平的降低以及功能的丧失参与了脑梗死的发生和发展,其机制可能与机体免疫平衡被打破有关。
Objective To investigate the level of peripheral blood regulatory B cells(Bregs)in patients with cerebral infarction and its correlation with the severity of carotid atherosclerosis.Methods Fifty patients with atherosclerotic cerebral infarction who were admitted to the Department of Neurology,Taihe Hospital from January 2017 to May 2018 were selected as the study group,and 50 healthy controls were selected as the control group.Flow cytometry(FCM)was used to detect the proportion of CD19+CD5+CD1 d+B cells(Bregs)in B cells.Interleukin-10(IL-10)and transforming growth factor-β1(TGF-β1)levels in supernatant of Bregs culture medium were determined by ELISA.Then we compared the data between the 50 healthy people and the 50 patients with cerebral infarction and carotid atherosclerosis.Results The levels of Bregs,IL-10 and TGF-β1 in the patients with cerebral infarction were significantly lower than those in the healthy people(P<0.05).As the severity of carotid atherosclerosis worsened,the levels of peripheral blood Bregs and the levels of cytokines IL-10 and TGF-β1 gradually decreased(P<0.05).Conclusions Decreased levels and loss of function of peripheral blood Bregs are involved in the development and progression of cerebral infarction,which may be related to the disruption of the body's immune balance.
Objective To investigate the level of peripheral blood regulatory B cells(Bregs)in patients with cerebral infarction and its correlation with the severity of carotid atherosclerosis.Methods Fifty patients with atherosclerotic cerebral infarction who were admitted to the Department of Neurology,Taihe Hospital from January 2017 to May 2018 were selected as the study group,and 50 healthy controls were selected as the control group.Flow cytometry(FCM)was used to detect the proportion of CD19+CD5+CD1 d+B cells(Bregs)in B cells.Interleukin-10(IL-10)and transforming growth factor-β1(TGF-β1)levels in supernatant of Bregs culture medium were determined by ELISA.Then we compared the data between the 50 healthy people and the 50 patients with cerebral infarction and carotid atherosclerosis.Results The levels of Bregs,IL-10 and TGF-β1 in the patients with cerebral infarction were significantly lower than those in the healthy people(P<0.05).As the severity of carotid atherosclerosis worsened,the levels of peripheral blood Bregs and the levels of cytokines IL-10 and TGF-β1 gradually decreased(P<0.05).Conclusions Decreased levels and loss of function of peripheral blood Bregs are involved in the development and progression of cerebral infarction,which may be related to the disruption of the body's immune balance.
引文
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[15]钟晓南,胡学强.脑卒中的免疫机制进展[J].中国神经免疫学和神经病学杂志,2011,18(06):435-437.
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[17]Emsley HC, Hopkins SJ.Acute ischaemic stroke and infection:recent and emerging concepts[J].Lancet Neurol,2008,7(4):341-353.
[18]Mccoll BW,Allan SM,Rothwell NJ.Systemic infection,inflammation and acute ischemic stroke[J].Neuroscience,2009,158(3):1049-1061.
[19]Bodhankar S,Chen Y,Vandenbark AA,et al.IL-10-producing B-cells limit CNS inflammation and infarct volume in experimental stroke[J].Metab Brain Dis,2013,28(3):375-386.
[20]Ren X,Akiyoshi K,Dziennis S,et al.Regulatory B cells limit CNS inflammation and neurologic deficits in murine experimental stroke[J].J Neurosci,2011,31(23):8556-8563.
[2]Li GW,Zheng GY,Li JG,et al.Relationship between carotid atherosclerosis and cerebral infarction[J].Chin Med Sci J,2010,25(1):32-37.
[3]Dahl A,Lund C,Russell D.Atherosclerosis and cerebral infarction[J].Tidsskr Nor Laegeforen,2007,127(7):892-896.
[4]Li JJ.Inflammation in coronary artery diseases[J].Chin Med J(Engl),2011,124(21):3568-3575.
[5]Tousoulis D, Kampoli AM, Papageorgiou N, et al.Pathophysiology of atherosclerosis:the role of inflammation[J].Curr Pharm Des,2011,17(37):4089-4110.
[6]Rosser EC,Mauri C.Regulatory B cells:origin,phenotype,and function[J].Immunity,2015,42(4):607-612.
[7]van de Veen W.The role of regulatory B cells in allergen immunotherapy[J].Curr Opin Allergy Clin Immunol,2017,17(6):447-452.
[8] Maravillas-Montero JL, Acevedo-Ochoa E. Human B regulatory cells:The new players in autoimmune disease[J].Rev Invest Clin,2017,69(5):243-246.
[9]Ren X,Akiyoshi K,Dziennis S,et al.Regulatory B cells limit CNS inflammation and neurologic deficits in murine experimental stroke[J]. J Neurosci,2011,31(23):8556-8563.
[10]Srikakulapu P,Mcnamara CA.B cells and atherosclerosis[J].Am J Physiol Heart Circ Physiol,2017,312(5):H1060-H1067.
[11]Lu H,Daugherty A.Regulatory B cells,interleukin-10,and atherosclerosis[J].Curr Opin Lipidol,2015,26(5):470-471.
[12]王建伟,陈红芳.中国急性缺血性脑卒中诊治指南新旧版本比较[J].浙江实用医学,2016,21(03):233-235.
[13]中华医学会神经病学分会脑血管病学组急性缺血性脑卒中诊治指南撰写组.中国急性缺血性脑卒中诊治指南2010[J].中国医学前沿杂志(电子版),2010,2(04):50-59.
[14]中华医学会神经病学分会,中华医学会神经病学分会脑血管病学组.中国急性脑缺血性脑卒中诊治指南2014[J].中华神经科杂志,2015,48(4):246-257.
[15]钟晓南,胡学强.脑卒中的免疫机制进展[J].中国神经免疫学和神经病学杂志,2011,18(06):435-437.
[16]Stoll G,Bendszus M.Inflammation and atherosclerosis:novel insights into plaque formation and destabilization[J].Stroke,2006,37(7):1923-1932.
[17]Emsley HC, Hopkins SJ.Acute ischaemic stroke and infection:recent and emerging concepts[J].Lancet Neurol,2008,7(4):341-353.
[18]Mccoll BW,Allan SM,Rothwell NJ.Systemic infection,inflammation and acute ischemic stroke[J].Neuroscience,2009,158(3):1049-1061.
[19]Bodhankar S,Chen Y,Vandenbark AA,et al.IL-10-producing B-cells limit CNS inflammation and infarct volume in experimental stroke[J].Metab Brain Dis,2013,28(3):375-386.
[20]Ren X,Akiyoshi K,Dziennis S,et al.Regulatory B cells limit CNS inflammation and neurologic deficits in murine experimental stroke[J].J Neurosci,2011,31(23):8556-8563.