血清与肺泡灌洗液TLR4及免疫功能指标对重症肺部感染患者生存状况的预测研究
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摘要
目的探讨血清与肺泡灌洗液Toll样受体4(TLR4)及免疫功能指标对重症肺部感染患者生存状况的预测效果。方法选择2013年1月-2018年1月在医院呼吸重症监护病房接受治疗的重症肺部感染患者166例,根据患者1个月内的生存状况,分为死亡组58例和生存组108例。分别对两组患者入院当天和入院1周后血清和肺泡灌洗液中的TLR4表达水平、免疫功能细胞CD_3~+、CD_4~+、CD_8~+T淋巴细胞、B淋巴细胞和自然杀伤细胞(natural killer cell,NK)的表达水平进行分析。结果两组患者入院时血清及肺泡灌洗液中TLR4表达水平比较差异无统计学意义,入院后1周,死亡组患者TLR4表达水平逐渐升高,生存组患者逐渐下降,比较差异有统计学意义(P<0.05);两组患者入院时免疫功能细胞CD_3~+、CD_4~+、CD_8~+T淋巴细胞、B淋巴细胞和NK细胞表达水平比较差异均无统计学意义,入院后1周死亡组患者上述免疫细胞表达水平逐渐下降,生存组患者无明显变化,且死亡组CD_3~+、CD_4~+、CD_8~+T淋巴细胞水平低于生存组(P<0.05)。结论 Toll样受体4的高表达,T淋巴细胞及其亚群的低表达可能造成重症肺部感染患者预后较差。
OBJECTIVE To explore the value of serum and alveolar lavage fluid Toll-like receptor(TLR4)and immune function indexes in prediction of survival status of patients with severe pulmonary infection.METHODS A total of 166 patients with severe pulmonary infection who were treated in respiratory intensive care unit from Jan 2013 to Jan 2018 were enrolled in the study and divided into the death group with 58 cases and the survival group according to the survival status within 1 month.The levels of serum and alveolar lavage fluid TLR4,CD_3~+,CD_4~+,CD_8~+ T lymphocytes,B-lymphocyte and natural killer cell(NK)were observed and compared between the two groups of patients at the admission and after the admission for 1 week.RESULTS There were no significant differences in the levels of serum and alveolar lavage fluid TLR4 between the two groups of patients at the admission,while the TLR4 level of the death group was gradually elevated after the admission for 1 week,the TLR4 level of the survival group was declined,and there was significant difference((P<0.05).There were no significant differences in the levels of immunologic function cells CD_3~+,CD_4~+,CD_8~+ T lymphocytes,B-lymphocyte and NK cell between the two groups of patients at the admission,while the levels of above immune cells were gradually declined in the death group after the admission for 1 week but did not change significantly in the survival group;the levels of CD_3~+,CD_4~+ and CD_8~+ T lymphocytes of the death group were significantly lower than those of the survival group(P<0.05).CONCLUSIONThe high expression of TLR4 and low expression of T lymphocyte and its subsets may lead to the poor prognosis of the patients with severe pulmonary infection.
OBJECTIVE To explore the value of serum and alveolar lavage fluid Toll-like receptor(TLR4)and immune function indexes in prediction of survival status of patients with severe pulmonary infection.METHODS A total of 166 patients with severe pulmonary infection who were treated in respiratory intensive care unit from Jan 2013 to Jan 2018 were enrolled in the study and divided into the death group with 58 cases and the survival group according to the survival status within 1 month.The levels of serum and alveolar lavage fluid TLR4,CD_3~+,CD_4~+,CD_8~+ T lymphocytes,B-lymphocyte and natural killer cell(NK)were observed and compared between the two groups of patients at the admission and after the admission for 1 week.RESULTS There were no significant differences in the levels of serum and alveolar lavage fluid TLR4 between the two groups of patients at the admission,while the TLR4 level of the death group was gradually elevated after the admission for 1 week,the TLR4 level of the survival group was declined,and there was significant difference((P<0.05).There were no significant differences in the levels of immunologic function cells CD_3~+,CD_4~+,CD_8~+ T lymphocytes,B-lymphocyte and NK cell between the two groups of patients at the admission,while the levels of above immune cells were gradually declined in the death group after the admission for 1 week but did not change significantly in the survival group;the levels of CD_3~+,CD_4~+ and CD_8~+ T lymphocytes of the death group were significantly lower than those of the survival group(P<0.05).CONCLUSIONThe high expression of TLR4 and low expression of T lymphocyte and its subsets may lead to the poor prognosis of the patients with severe pulmonary infection.
引文
[1]董朝辉,谢艳萍,陈志冬,等.纤维支气管镜联合肺泡灌洗术治疗重症肺部感染患者的临床疗效[J].中华医院感染学杂志,2018,28(3):364-367.
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[12]刘曙艳,周雪红,陈洁.胰岛素泵强化治疗糖尿病并重症肺部感染及对血清和肺泡灌洗液中炎症因子的影响[J].中国现代医学杂志,2018,28(3):107-112.
[13]王巍,鹿翠香,何平,等.纤维支气管镜吸痰辅助治疗对重症肺部感染患者的疗效及炎症标志物水平的影响分析[J].中华医院感染学杂志,2017,27(22):5083-5086.
[14]Hong G,Kim DH,Kim YS.Successful treatment of acute respiratory failure in a patient with pulmonary Mycobacterium abscessus infection accompanied by oganizing pneumonia[J].JThorac Dis,2017,9(6):E560-E564.
[15]Wang H,Anthony D,Yatmaz S,et al.Aspirin-triggered resolvin D1reduces pneumococcal lung infection and inflamation in a viral and bacterial coinfection pneumonia model[J].Clin Sci(Lond),2017,131(18):2347-2362.
[16]Hanen S,Najwane SS,Abir Z,et al.Chlamydia trachomatis infection increases the expression of inflammatory tumorigenic cytokines and chemokines as well as components of the Toll-like receptor and NF-κB pathways in human prostate epithelial cells[J].Mol Cell Probes,2014,28:147-154.
[17]李丛哲,吴利先,王国富.Toll样受体4在结核分枝杆菌感染中的作用和研究进展[J].中国病原生物学杂志,2017,12(4):378-380.
[18]Verweij SP,Karimi O,Pleijster J,et al.TLR2,TLR4and TLR9genotypes and haplotypes in the susceptibility to and clinical course of Chlamydia trachomatis infections in Dutch women[J].Pathog Dis,2016,74(1):107-110.
[19]Previte DM,O'Connor EC,Novak EA,et al.Reactive oxygen species are required for driving efficient and sustained aerobic glycolysis during CD4+T cell activation[J].PLoS One,2017,12(4):e0175549.
[20]Dumke R,Schnee C,Pletz MW,et al.Mycoplasma pneumoniae and Chlamydia spp.infection in community-acquired pneumonia,Germany,2011-2012[J].Emerg Infect Dis,2015,21(3):426-434.
[21]Agrawal T,Bhengraj AR,Vats V,et al.Expression of TLR2,TLR4and iNOS in cervical monocytes of Chlamydia trachomatis infected women and their role in host immune response[J].Am J Reproduct Immunol,2011,66(6):534-543.
[22]Ding Y,Yang KL,Xiang W,et al.CD200RI agonist attenuates induced inflammatory response in human renal proximal tubular epithelial cells by regulating TLR4-MyD88-TAKlmediated NF-kappa B and MAPK pathway[J].Biochem Biopbys Rcs Commun,2015,460(2):287-294.
[23]Rocca YS,Roberti MP,Arriaga JM,et al.Altered phenotype in peripheral blood and tumor-associated NK cells from colorectal cancer patients[J].Innate Immun,2013,19(1):76-85.
[24]Thomas BJ,Kan-O K,Loveland KL,et al.In the shadow of fibrosis:innate immune suppression mediated by transforming growth factor-β[J].Am J Respir Cell Mol Biol,2016,55(6):759-766.
[25]赵丹,宁睿,王春艳,等.不同预后的重症肺炎患者住院期间血清和肺泡灌洗液TLR4水平、外周血免疫细胞计数比较[J].山东医药,2017,57(15):96-98.
[2]沈秀秀,刘芋兵,郑婷婷,等.重症肺部感染患者DIC评分系统与CRP变化对并发急性肾损伤的预测价值[J].中华医院感染学杂志,2018,28(2):177-179.
[3]Yanik G,Grupp S,Pulsipher MA,et al.Competitive TNF inhibitor(ETANERCEPT)for the treatment of idiopathic pneumonia syndrome(IPS)following allogeneic stem cell transplantation(SCT).A joint Pediatric Blood and Marrow Transplant Consortium(PBMTC)and Childrens Oncology Group(COG)Study[J].Biol Blood Marrow Transplant,2013,19(2):109-112.
[4]Bruhn KW,Pantapalangkoor P,Nielsen T,et al.Host fate is rapidly determined by innate effector-microbial interactions during Acinetobacter baumannii bacteremia[J].J Infect Dis,2015,211(8):1296-1305.
[5]Ho MC,Ker CR,Hsu JH,et al.Usefulness of lung ultrasound in the diagnosis of community-acquired pneumonia in children[J].Pediatr Neonatol,2015,56(1):40-45.
[6]陈凯.重症肺部感染患者采取纤维支气管镜吸痰联合肺泡灌洗的临床效果[J].中国医学工程,2018,26(1):64-66.
[7]Iwasaki A,Medzhitov R.Toll-like receptor control of the adaptive immune responses[J].Nat Immunol,2004,5(10):987-995.
[8]Li S,Huang X,Chen Z,et al.Neutrophil CD64expression as a biomarker in the early diagnosis of bacterial infection:a meta-analysis[J].Int J Infect Dis,2013,17(1):e12-e23.
[9]Saraya T,Kurai D,Nakagaki K,et al.Novel aspects on the pathogenesis of Mycoplasma pneumoniae pneumonia and therapeutic implications[J].Front Microbiol,2014,5(12):410-415.
[10]Zhang H,Chen Z,Liu H.Pathogenic mechanism of Mycoplasma pneumoniae infections[J].Chin J Pediatr,2016,54(2):94-97.
[11]张海邻,陈志敏,刘瀚曼,等.肺炎支原体感染的致病机制[J].中华儿科杂志,2016,54(2):94-97.
[12]刘曙艳,周雪红,陈洁.胰岛素泵强化治疗糖尿病并重症肺部感染及对血清和肺泡灌洗液中炎症因子的影响[J].中国现代医学杂志,2018,28(3):107-112.
[13]王巍,鹿翠香,何平,等.纤维支气管镜吸痰辅助治疗对重症肺部感染患者的疗效及炎症标志物水平的影响分析[J].中华医院感染学杂志,2017,27(22):5083-5086.
[14]Hong G,Kim DH,Kim YS.Successful treatment of acute respiratory failure in a patient with pulmonary Mycobacterium abscessus infection accompanied by oganizing pneumonia[J].JThorac Dis,2017,9(6):E560-E564.
[15]Wang H,Anthony D,Yatmaz S,et al.Aspirin-triggered resolvin D1reduces pneumococcal lung infection and inflamation in a viral and bacterial coinfection pneumonia model[J].Clin Sci(Lond),2017,131(18):2347-2362.
[16]Hanen S,Najwane SS,Abir Z,et al.Chlamydia trachomatis infection increases the expression of inflammatory tumorigenic cytokines and chemokines as well as components of the Toll-like receptor and NF-κB pathways in human prostate epithelial cells[J].Mol Cell Probes,2014,28:147-154.
[17]李丛哲,吴利先,王国富.Toll样受体4在结核分枝杆菌感染中的作用和研究进展[J].中国病原生物学杂志,2017,12(4):378-380.
[18]Verweij SP,Karimi O,Pleijster J,et al.TLR2,TLR4and TLR9genotypes and haplotypes in the susceptibility to and clinical course of Chlamydia trachomatis infections in Dutch women[J].Pathog Dis,2016,74(1):107-110.
[19]Previte DM,O'Connor EC,Novak EA,et al.Reactive oxygen species are required for driving efficient and sustained aerobic glycolysis during CD4+T cell activation[J].PLoS One,2017,12(4):e0175549.
[20]Dumke R,Schnee C,Pletz MW,et al.Mycoplasma pneumoniae and Chlamydia spp.infection in community-acquired pneumonia,Germany,2011-2012[J].Emerg Infect Dis,2015,21(3):426-434.
[21]Agrawal T,Bhengraj AR,Vats V,et al.Expression of TLR2,TLR4and iNOS in cervical monocytes of Chlamydia trachomatis infected women and their role in host immune response[J].Am J Reproduct Immunol,2011,66(6):534-543.
[22]Ding Y,Yang KL,Xiang W,et al.CD200RI agonist attenuates induced inflammatory response in human renal proximal tubular epithelial cells by regulating TLR4-MyD88-TAKlmediated NF-kappa B and MAPK pathway[J].Biochem Biopbys Rcs Commun,2015,460(2):287-294.
[23]Rocca YS,Roberti MP,Arriaga JM,et al.Altered phenotype in peripheral blood and tumor-associated NK cells from colorectal cancer patients[J].Innate Immun,2013,19(1):76-85.
[24]Thomas BJ,Kan-O K,Loveland KL,et al.In the shadow of fibrosis:innate immune suppression mediated by transforming growth factor-β[J].Am J Respir Cell Mol Biol,2016,55(6):759-766.
[25]赵丹,宁睿,王春艳,等.不同预后的重症肺炎患者住院期间血清和肺泡灌洗液TLR4水平、外周血免疫细胞计数比较[J].山东医药,2017,57(15):96-98.