全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...
-  2017 

调节性T细胞在烟熏诱导的小鼠肺气肿模型中的变化及意义 Change and Significance of Regulatory T Cells in Emphysema Model Mice Induced by Smoking

Keywords: COPD,自身免疫,调节性T细胞

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的:研究CD4~+Foxp3~+调节性T细胞在烟熏诱导的小鼠肺气肿模型中的变化并探讨其意义。方法:6-8周龄C57BL/6FoxP3-GFP knock-in小鼠18只,按照随机对照方法分为吸烟组(S组)和非吸烟组(NS组),将吸烟组小鼠暴露自制烟熏箱里,每天烟熏4h,每周烟熏5d,连续24周建立小鼠肺气肿模型,正常对照组小鼠置入空气清洁的房间。24周后取两组小鼠的肺组织进行HE染色评价肺气肿,同时通过流式细胞术检测小鼠支气管肺泡灌洗液、肺组织、纵隔淋巴结、脾脏中Treg细胞、CD4~+T细胞、CD8~+T细胞、CD4~+CD69~+T细胞、CD8~+CD69~+T细胞的数量变化。结果:与非吸烟鼠相比,烟熏24周后吸烟鼠肺组织的病理染色可见典型肺气肿表现;吸烟鼠肺组织、支气管肺泡灌洗液及纵隔淋巴结中Treg细胞、CD4~+T细胞、CD8~+T细胞及其活化细胞(即CD4~+CD69~+T细胞和CD8~+CD69~+T细胞)的数量明显高于非吸烟鼠,差异有统计学意义(P<0.05),而上述细胞在两组小鼠的脾脏中的数量无明显差异(P>0.05)。结论:吸烟鼠肺组织、支气管肺泡灌洗液及纵隔淋巴结中Treg细胞、CD4~+T细胞、CD8~+T细胞及其活化细胞的数量明显高于非吸烟鼠,提示小鼠肺气肿模型中存在将累及肺组织及其周围组织的异常炎症反应,而淋巴细胞可能在其中发挥了重要作用,而由于Treg细胞相对不足或功能障碍使其不能正常发挥免疫调节作用

References

[1]  Hogg JC.Pathophysiology of airflow limitation in chronic obstructive pulmonary disease[J].Lancet,2004,364(9435):709-721.
[2]  Smyth LJ,Starkey C,Vestbo J,et al.CD4-regulatory cells in COPD patients[J].Chest,2007,132(1):156-163.
[3]  Vargas-Rojas MI,Ramirez-Venegas A,Limon-Camacho L,et al.Increase of Th17cells in peripheral blood of patients with chronic obstructive pulmonary disease[J].Respir Med,2011,105(11):1 648-1 654.
[4]  Plumb J,Smyth LJ,Adams HR,et al.Increased Tregulatory cells within lymphocyte follicles in moderate COPD[J].Eur Respir J,2009,34(1):89-94.
[5]  Pages F,Ragueneau M,Rottapel R,et al.Binding of phosphatidylinositol-3-OH kinase to CD28is required for T-cell signalling[J].Nature,1994,369(6478):327-329.
[6]  Kohansal R,Martinez-Camblor P,Agusti A,et al.The natural history of chronic airflow obstruction revisited:an analysis of the Framingham offspring cohort[J].Am J Respir Crit Care Med,2009,180(1):3-10.
[7]  Hogg JC,Chu F,Utokaparch S,et al.The nature of small-airway obstruction in chronic obstructive pulmonary disease[J].N Engl J Med,2004,350(26):2 645-2 653.
[8]  Saetta M,Turato G,Maestrelli P,et al.Cellular and structural bases of chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,2001,163(6):1 304-1 309.
[9]  Lee SH,Goswami S,Grudo A,et al.Antielastin autoimmunity in tobacco smoking-induced emphysema[J].Nat Med,2007,13(5):567-569.
[10]  Feghali-Bostwick CA,Gadgil AS,Otterbein LE,et al.Autoantibodies in patients with chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,2008,177(2):156-163.
[11]  Nunez B,Sauleda J,Anto JM,et al.Anti-tissue antibodies are related to lung function in chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,2011,183(8):1 025-1 031.
[12]  O'Shaughnessy TC,Ansari TW,Barnes NC,et al.Inflammation in bronchial biopsies of subjects with chronic bronchitis:inverse relationship of CD8+T lymphocytes with FEV1[J].Am J Respir Crit Care Med,1997,155(3):852-857.
[13]  Saetta M,Di Stefano A,Turato G,et al.CD8+Tlymphocytes in peripheral airways of smokers with chronic obstructive pulmonary disease[J].Am J Respir Crit Care Med,1998,157(3Pt 1):822-826.
[14]  Saetta M,Baraldo S,Turato G,et al.Increased proportion of CD8+T-lymphocytes in the paratracheal lymph nodes of smokers with mild COPD[J].Sarcoidosis Vasc Diffuse Lung Dis,2003,20(1):28-32.
[15]  Turato G,Zuin R,Miniati M,et al.Airway inflammation in severe chronic obstructive pulmonary disease:relationship with lung function and radiologic emphysema[J].Am J Respir Crit Care Med,2002,166(1):105-110.
[16]  Ziegler SF,Ramsdell F,Alderson MR.The activation antigen CD69[J].Stem Cells,1994,12(5):456-465.
[17]  Voelkel N,Taraseviciene-Stewart L.Emphysema:an autoimmune vascular disease[J].Proc Am Thorac Soc,2005,2(1):23-25.
[18]  Agusti A,Macnee W,Donaldson K,et al.Hypothesis:does COPD have an autoimmune component[J].Thorax,2003,58(10):832-834.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133