慢性阻塞性肺疾病（COPD）是一种常见病、多发病，其发病率和死亡率均较高，严重影响人类健康及生活质量。细菌等感染及机体自身免疫功能紊乱等因素共同参与COPD的发病过程。COPD本质上是一种慢性系统性炎症疾病，机体炎症介质变化是衡量慢性阻塞性肺疾病急性加重期（AECOPD）感染程度的重要指标，尤其是T细胞介导的免疫炎症反应，在AECOPD的发病过程中占据重要地位。血清IL-17和IL-10作为评估机体免疫状态的炎症介质，参与AECOPD的发病过程。血清肝素结合蛋白是COPD患者在感染状态下释放的一种炎症介质，参与机体一系列的炎症反应。研究机体内3种炎症介质的变化特点对研究AECOPD的发生发展过程、判断病情的严重程度以及指导临床用药等方面具有重要的临床意义，为积极探索COPD新的诊疗靶点提供重要的理论依据。

[1] LIANG R,ZHANG W,SONG Y M.Levels of leptin and IL-6 in lungs and blood are associated with the severity of chronic obstructive pulmonary disease in patients and rat models[J].Mol Med Rep,2013,7:1470-1476.
[2] DESAI H,ESCHBERGER K,WRONA C,et al.Bacterial colonization increases daily symptoms in patients with chronic obstructive pulmonary disease[J].Ann Am Thorac Soc,2014,11(3):303-309.
[3] SHANMUGAM L,JOHNSON P,KINDO A J,et al.Assessment of phagocytic activity of neutrophils in chronic obstructive pulmonary disease[J].Lung India,2015,32(5):437-440.
[4] ZHANG J Q,CHU S Y,ZHONG X N,et al.Increased expression of CD4+IL-17+ cells in the lung tissue of patients with stable chronic obstructive pulmonary disease (COPD) and smokers[J].Int Immunopharmacol,2013,15(1):58-66.
[5] IWAKURA Y,ISHIGAME H,SAIJO S,et al.Functional specialization of interleukin-17 family members[J].Immunity,2011,34(2):149-162.
[6] SINGH D.Chronic obstructive pulmonary disease,neutrophils and bacterial infection:a complex web involving IL-17 and IL-22 unravels[J].EBioMedicine,2015,2(11):1580-1581.
[7] VANAUDENAERDEVB M,VERLEDEN S E,VOS R,et al.Innate and adaptive IL-17 producing lymphocytes in chronic inflammatory lung disorders[J].Am J Respir Crit Care Med,2011,183(8):977-986.
[8] CHANG Y,NADIGEL J,BOULAIS N,et al.CD8 positive T cells express IL-17 in patients with chronic obstructive pulmonary disease[J].Respir Res,2011,12(1):43.
[9] RANGANATH S,BHANDARI A,MCMAHON J,et al.Discovery and characterization of a potent interleukin-6 binding peptide with neutralizing activity in vivo[J].PLoS One,2015,10(11):e0141330.
[10] HIGAKI M,WADA H,MIKURA S,et al.Interleukin-10 modulates pulmonary neutrophilic inflammation induced by cigarette smoke exposure[J].Exp Lung Res,2015,41(10):525-534.
[11] WANG H Y,YING H J,WANG I S,et al.mbalance of peripheral blood Th17 and Treg responses in patients with chronic obstructive pulmonary disease[J].Clin Respir J,2015,9(3):330-341.
[12] IMANI S,SALIMIAN J,BOZORGMEHR M,et al.Assessment of Treg/Th17 axis role in immunopathogenesis of chronic injuries of mustard lung disease[J].J Recept Signal Transduct Res,2016,36(5):531-541.
[13] TAPPER H,KARLSSON A,FLODAARD H,et al.Secretion of heparin-binding protein from human neutrophils is determined by its localization in azurophilic granules and secretory vesicles[J].Blood,2002,99(5):1785-1793.
[14] CHEW M S,LINDER A,SANTEN S,et al.Increased plasma levels of heparin-binding protein in patients with shock:a prospective,cohort study[J].Inflamm Res,2012,61(4):375-379.
[15] KAUKONEN K M,LINDBOM L,HERWALD H,et al.Heparin binding protein in patients with acute respiratory failure treated with granulocyte colony-stimulating factor (filgrastim)-a prospective,placebo-controlled,double-blind study[J].BMC Infect Dis,2013,13:51.
[16] LINDER A,AKESSON P,INGHAMMAR M,et al.Elevated plasma levels of heparin-binding protein in intensive care unit patients with severe sepsis and septic shock[J].Crit Care,2012,16(3):R90.
[17] 陈淑芳,陈复辉,刘晶,等.慢性阻塞性肺疾病的免疫治疗进展[J].现代医学,2016,44(10):1468-1471.