摘要
目的探讨吸烟对慢性阻塞性肺疾病(COPD)患者肺部微结构以及血清TREG/TH17的影响观察。方法选择东莞市第五人民医院2016年5月—2017年4月的COPD患者84例作为研究组,分为吸烟组44例,不吸烟组40例。选取同期的健康体检人群80例作为对照组,分为吸烟组40例,不吸烟组40例。比较两组患者的肺部微结构及血清TREG/TH17。结果研究组的吸烟患者相对于对照组吸烟患者肺微生态菌群失调,导致肺免疫紊乱,进而引发炎症浸润,导致COPD发病。研究组的吸烟者与对照组的吸烟者血清TREG/TH17细胞比例分别为(3.24±0.84)%和(2.06±0.38)%,两组比较差异有统计学意义(P<0.05);研究组的非吸烟者与对照组的非吸烟者血清TREG/TH17细胞比例分别为(2.96±0.92)%和(1.94±0.32)%,两组间差异有统计学意义(P<0.05)。结论吸烟与COPD患者的血清TREG/TH17细胞比例相关,吸烟引起了血清TREG/TH17细胞比例失衡进而导致COPD的发生发展。
引文
[1]PAUWELS R A,BUIST A S,CALVERLEY P M,et al.Global strategy for the diagnosis,management,and prevention of chronic obstructive pulmonary disease.NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease(GOLD)workshop summary[J].Am J Rspir Crit Care Med,2001,163:1256-1276.
[2]CELLI B R,MAC NEE W,AGUSTI A,et al.Standards for the diagnosis and treatment of patients with COPD:a summary of the ATS/ERS position paper[J].Eur Respir J,2004,23:932-946.
[3]LOUTEN J,BONIFACE K,DE WAAL MALEFYT R.Devel‐opment and function of TH17 cells in health and disease[J].JAllergy Clin Immunol,2009(123):1004-1011.
[4]AGUSTI A,MACNEE W,DONALDSON K,et al.Hypothesis:does COPD have an autoimmune component[J].Thorax,2003(58):832-834.
[5]BARNES P J.Immunology of asthma and chronic obstructive pulmonary disease[J].Nat Rev Immunol,2008(8):183-192.
[6]HILTY M,BURKE C,PEDRO H,et al.Disordered microbial communities in asthmatic airways[J].Plos One,2010,5(1):e8578.
[7]MARTIN C,BURGEL P R,LEPAGE P,et al.Host-microbe interactions in distal airways:relevance to chronic airways dis‐easea[J].Eur Respir Rev,2015,24(135):78-91.
[8]ERB-DOWNWARD J R,THOMPSON D L,HAN M K,et al.Analysis of the lung microbiome in the“healthy”smoker and in COPD[J].Plos One,2011,6(2):e16384.
[9]BETTELI E,KORN T,OUKKA M,et al.Induction and ef‐fector functions of T(H)17 cells[J].Nature,2008,453:1051-1057.
[10]VARGAS-ROJAS M I,RAMIREZ-VENEGAS A,LIMON-CAMACHO L,et al.Increase of Th17 cells in peripheral blood of patients with chronic obstructive pulmonary disease[J].Respir Me,2011,105(11):1648-1654.
[11]KORN T,BETTELLI E,GAO W,et al.IL-21 initiates an alternative pathway to induce proinflammatory T(H)17 cells[J].Nature,2007,448:484-487.
[12]BARCELO B,PONS J,FERRER J M,et al.Phenotypic characterization of T-lymphocytes in COPD:abnormal CD4+CD25+regulatory T-lymphocyte response to tobacco smoking[J].Eur Respir J,2008,31(3):555-562.