摘要
目的探究结核病感染期间中性粒细胞CD64、TLR2和TLR4表达变化分析其对免疫反应造成的影响。方法筛取2016年10月至2018年3月来该院呼吸内科就诊的患者,按患者是否患有结核病分为对照组(n=38)和观察组(n=36),分别检测感染结核分枝杆菌前后其外周血中中性粒细胞和Toll样受体(TLRs)的表达水平,检测中性粒细胞吞噬作用变化。结果两组感染后CD64表达水平均明显高于感染前且观察组均高于对照组,差异有统计学意义(P<0.05);对照组感染后CD32表达水平明显提升,差异有统计学意义(P<0.05);对照组感染前TLRs表达水平均明显低于观察组,差异有统计学意义(P<0.05),感染后两组TLRs表达量均明显下降,差异有统计学意义(P<0.05);两组感染前后中性粒细胞吞噬作用百分比均明显变化,差异有统计学意义(P<0.05),感染前对照组吞噬作用百分比明显高于观察组,差异有统计学意义(P<0.05)。结论结核病感染期间,患者外周血中性粒细胞CD64、TLR2和TLR4表达水平均明显升高,且中性粒细胞吞噬功能下降明显。
引文
[1]FALZON D,SCHNEMANN H J,HARAUSZ E,et al.World Health Organization treatment guidelines for drug-resistant tuberculosis,2016update[J].Eur Respir J,2017,49(3):1602308.
[2]WANG J,HOSSAIN M,THANABAL A,et al.Visualizing the function and fate of neutrophils in sterile injury and repair[J].Science,2017,358(6359):111-115.
[3]NAVEGANTES K C,GOMES R D,TARTARI P A,et al.Immune modulation of some autoimmune diseases:the critical role of macrophages and neutrophils in the innate and adaptive immunity[J].J Transl Med,2017,15(1):36-57.
[4]FARIDGOHAR M,NIKOUEINEJAD H.New findings of Toll-like receptors involved in Mycobacterium tuberculosis infection[J].Pathog Glob Health,2017,111(5):256-264.
[5]DALLENGA T,REPNIK U,CORLEIS B,et al.M-tuberculosis-induced necrosis of infected neutrophils promotes bacterial growth following phagocytosis by macrophages[J].Cell Host Mic,2017,22(4):519-530.
[6]张庭艳,关瑞莲,梁红,等.中性粒细胞CD64对新生儿感染早期判断的研究[J].实用医学杂,2016,32(13):2205-2208.
[7]陈静思,孙晨,阳海平,等.过敏性紫癜患者中性粒细胞及其IgA Fc受体对血管内皮细胞凋亡的影响及机制[J].中华皮肤科杂志,2017,50(11):795-799.
[8]陆姗姗,陈益国,张咏,等.TLR2配基Pam3CSK4对小鼠中性粒细胞吞噬耐甲氧西林金黄色葡萄球菌功能的影响[J].现代预防医学,2018,20(8):1453-1457.
[9]胥江俊,胡屹,蒋伟利,等.上海市流动人口肺结核患者密切接触者结核分枝杆菌潜伏感染情况及危险因素[J].中华结核和呼吸杂志,2016,39(1):25-29.
[10]CLARK S,LANNI F,MARINOVA D,et al.Revaccination of Guinea Pigs with the live attenuated mycobacterium tuberculosis vaccine MTBVAC improves BCG′s protection against tuberculosis[J].J Infect Dis,2017,216(5):525-533.
[11]MARAIS B J,SINTCHENKO V.Epidemic spread of multidrug-resistant tuberculosis in China[J].Lancet Infect Dis,2017,17(3):238-239.
[12]AWONIYI D O,TEUCHERT A,SUTHERLAND J S,et al.Evaluation of cytokine responses against novel Mtb antigens as diagnostic markers for TB disease[J].J Infect,2016,73(3):219-230.
[13]GU X,GAO Y,MU D G,et al.MiR-23a-5p modulates mycobacterial survival and autophagy during mycobacterium tuberculosis infection through TLR2/MyD88/NF-kB pathway by targeting TLR2[J].Exp Cell Res,2017,354(2):71-77.
[14]ALARIDAH N,WINQVIST N,HAKANSSON G,et al.Impaired CXCR1-dependent oxidative defence in active tuberculosis patients[J].Tubercul,2015,95(6):744-750.
[15]RONNELID J.Granulocyte-augmented chemokine production induced by typeⅡcollagen-containing immune complexes is mediated via TLR4in rheumatoid arthritis patients[J].Europ J Immunol,2016,46(12):2822-2834.