重症甲型流感肺炎患儿血清细胞因子的检测及其临床意义
|
摘要
目的观察重症甲型流感肺炎患儿外周血细胞因子变化与临床意义。方法收集重症甲型流感患儿43例作为观察组,同时选取同期入住的室重症非流感病毒性肺炎患儿30例作为对照组,入院时对两组进行危重症评分,检测外周血IL-2、IL-4、IL-6、IL-8、IL-10、TNF、IFN水平。结果观察组除1例死亡,其余均病情好转后转入普通病房继续治疗,对照组无死亡病例;与对照组相比,观察组患儿血清细胞因子IL-6、IFN水平增高明显,差异均有统计学意义(均P<0.05);而IL-2、IL-4、IL-10、TNF差异均无统计学意义(均P>0.05)。结论与病毒性肺炎相比,重症甲型流感肺炎患儿血清IL-6、IL-10水平明显增高,存在免疫功能状态紊乱。
Objective To observe the changes and clinical significance of peripheral blood cytokines in children with severe influenza A pneumonia. Methods 43 children with severe influenza A admitted to PICU(observation group) and30 children with severe non-influenza virus pneumonia admitted to paediatric department(control group) were enrolled.They all were assessed with critical illness score. Peripheral blood IL-2、IL-4、IL-6、IL-8、IL-10、TNF and IFN were measured. Results Except for one death in the observation group,all patients were transferred to the general ward for continuous treatment after their condition improved. There was no death in the control group. Compared with the control group, serum levels of cytokines IL-6 and IFN were significantly increased in the observation group(P <0.05). No significant difference of IL-2, IL-4, IL-10 and TNF was found between the two groups. Conclusion There is a disorder of immune function in children with severe influenza A pneumonia.
Objective To observe the changes and clinical significance of peripheral blood cytokines in children with severe influenza A pneumonia. Methods 43 children with severe influenza A admitted to PICU(observation group) and30 children with severe non-influenza virus pneumonia admitted to paediatric department(control group) were enrolled.They all were assessed with critical illness score. Peripheral blood IL-2、IL-4、IL-6、IL-8、IL-10、TNF and IFN were measured. Results Except for one death in the observation group,all patients were transferred to the general ward for continuous treatment after their condition improved. There was no death in the control group. Compared with the control group, serum levels of cytokines IL-6 and IFN were significantly increased in the observation group(P <0.05). No significant difference of IL-2, IL-4, IL-10 and TNF was found between the two groups. Conclusion There is a disorder of immune function in children with severe influenza A pneumonia.
引文
[1]何颜霞,马科伟.重症流感的肺外并发症[J].中华实用儿科临床杂志,2017,32(18)∶1370-1374.DOI∶10.3760/cma.j.issn.2095-428X.2017.18.003.
[2]江载芳,申昆玲,沈颖.诸福棠实用儿科学[M].8版.北京∶人民卫生出版社,2015∶1255-1262.
[3]国家卫生和计划生育委员会,国家中医药管理局.流行性感冒诊疗方案(2018年版)[J].中国感染控制杂志,2018,17(2)∶181-184.DOI∶10.3969/j.issn.1671-9638.2018.02.020.
[4]中华医学会儿科学分会呼吸学组,《中华实用儿科临床杂志》编辑委员会.儿童流感诊断与治疗专家共识(2015年版)[J].中华实用儿科临床杂志,2015,30(17)∶1296-1303.DOI∶10.3760/cma.j.issn.2095-428X.2015.17.00.
[5]Pleschka S.0verview of influenza viruses[J].Curr Top Microbiol Immunol,2013,370∶1-20.DOI∶10.1007/82.2012.272.
[6]WHO.Innuenza(seasonal)[EB/0L].http://www.who.int//media-centre/factsheets/fs211/en/.
[7]杨静,陈涛,祝菲,等.2017~2018年度中国大陆流行性感冒病例报告情况分析[J].热带病与寄生虫病学,2018,16(2)∶63-66.DOI∶10.3969/j.issn.1672-2302.2018.02.001.
[8]Van Riel D,Munster VJ,de Wit E,et al.Hnnlan and avian influenza viruses target different ceils in the lower respiratory tract of humans and other mammals[J].Am J Pathol,2007,171(4)∶1215-1223.DOI∶10.2353/Ajpath.2007.070248.
[9]姚娜,李树德,王文林.IL-6,IL-10在实验性肺部炎症中的研究进展[J].昆明医科大学学报,2014,35(3)∶161-163.
[10]董智旻,童朝阳,姚晨,等.脓毒症患者细胞因子动态变化和免疫状态分型[J].中华急诊医学杂志,2017,26(2)∶149-154.DOI∶10.3760/cma.J.issn.1671-0282.2017.02.006.
[11]Xuelian Yu,Xi Zhang,Baihui Zhao,et al.Intensive Cytokine induction in Pandemic H1N1 Influenza Virus Infection Accompanied by Robust Production of IL-10 and IL-6[J].PLo S One,2011,6(12)∶e28680.DOI∶10.1371/journal.pone.0028680.
[12]Percopo CM,Ma M,Brenner TA,et al.Critical Adverse Impact of IL-6 in Acute Pneumovirus Infection[J].J Immunol,2019,202(3)∶871-882.DOI∶10.4049/jimmunol.1800927.
[13]Radigan KA,Nicholson TT,Welch LC,et al.Influenza A Virus Infection Induces Muscle Wasting via IL-6 Regulation of the E3Ubiquitin Ligase Atrogin-1[J].J Immunol,2019,202(2)∶484-493.DOI∶10.4049/jimmunol.1701433.
[14]Ramos JM,Garcia-Navarro M,Moreno V,et al.Interleukin(IL)-1β,IL-6 and tumor necrosis factor in patients with seasonal flu[J].Rev Esp Quimioter,2018,31(6)∶542-545.
[15]孙子梅.血清细胞因子检测在儿童肺炎支原体肺炎诊治中的意义[J].海南医学院学报,2016,22(3)∶273-275.DOI∶10.13210/j.enki.jhmu.20151030.01.
[16]Patel JA,Nair S,Ochoa EE,et a1.Interleukin-6-174 and tumor necrosis factorɑ-308 polymorphisms enhance cytokine production by human macrophages exposed torespiratory viruses[J].Interferon Cytokine Res,2010,30(12)∶917-921.DOI∶10.1089/jir.2010.0033.
[17]郑晶晶,顾玉海.低氧条件下IL-6、IL-8、IL-10作用机制研究进展[J].国际呼吸杂志,2016,36(3)∶224-227.DOI∶10.3760/cma.j.issn.1673-436X.2016.03.014.
[18]Chang WJ,Du Y,Zhao X,et al.Inflammation-related factors predicting prognosis of gastric cancer[J].World J Gastroenterol,2014,20(16)∶4586-4596.DOI∶10.3748/wjg.v20.i16.4586.
[19]Cai M,Zhang X,Li Y,et al.Toll-like receptor3 activation drives the inflammatory response in oxygen-induced retinopathy in rats[J].Br J Ophthalmol,2015,99(1)∶125-132.DOI∶10.1136/bjophthalmol-2014-305690.
[20]宋振举,童朝阳.严重脓毒症免疫调节治疗∶从免疫抑制走向免疫增强[J].中华急诊医学杂志,2014,23(4)∶365-368.DOI∶10.3760/cma.j.issn.1671-0282.2014.04.001.
[21]温前宽,李彦,杨建萍,等.严重脓毒症患者炎症因子的动态变化及预后意义[J].中华急诊医学杂志,2015,24(7)∶779-783.DOI∶10.3760/cma.j.issn.1671-0282.2015.07.020.
[2]江载芳,申昆玲,沈颖.诸福棠实用儿科学[M].8版.北京∶人民卫生出版社,2015∶1255-1262.
[3]国家卫生和计划生育委员会,国家中医药管理局.流行性感冒诊疗方案(2018年版)[J].中国感染控制杂志,2018,17(2)∶181-184.DOI∶10.3969/j.issn.1671-9638.2018.02.020.
[4]中华医学会儿科学分会呼吸学组,《中华实用儿科临床杂志》编辑委员会.儿童流感诊断与治疗专家共识(2015年版)[J].中华实用儿科临床杂志,2015,30(17)∶1296-1303.DOI∶10.3760/cma.j.issn.2095-428X.2015.17.00.
[5]Pleschka S.0verview of influenza viruses[J].Curr Top Microbiol Immunol,2013,370∶1-20.DOI∶10.1007/82.2012.272.
[6]WHO.Innuenza(seasonal)[EB/0L].http://www.who.int//media-centre/factsheets/fs211/en/.
[7]杨静,陈涛,祝菲,等.2017~2018年度中国大陆流行性感冒病例报告情况分析[J].热带病与寄生虫病学,2018,16(2)∶63-66.DOI∶10.3969/j.issn.1672-2302.2018.02.001.
[8]Van Riel D,Munster VJ,de Wit E,et al.Hnnlan and avian influenza viruses target different ceils in the lower respiratory tract of humans and other mammals[J].Am J Pathol,2007,171(4)∶1215-1223.DOI∶10.2353/Ajpath.2007.070248.
[9]姚娜,李树德,王文林.IL-6,IL-10在实验性肺部炎症中的研究进展[J].昆明医科大学学报,2014,35(3)∶161-163.
[10]董智旻,童朝阳,姚晨,等.脓毒症患者细胞因子动态变化和免疫状态分型[J].中华急诊医学杂志,2017,26(2)∶149-154.DOI∶10.3760/cma.J.issn.1671-0282.2017.02.006.
[11]Xuelian Yu,Xi Zhang,Baihui Zhao,et al.Intensive Cytokine induction in Pandemic H1N1 Influenza Virus Infection Accompanied by Robust Production of IL-10 and IL-6[J].PLo S One,2011,6(12)∶e28680.DOI∶10.1371/journal.pone.0028680.
[12]Percopo CM,Ma M,Brenner TA,et al.Critical Adverse Impact of IL-6 in Acute Pneumovirus Infection[J].J Immunol,2019,202(3)∶871-882.DOI∶10.4049/jimmunol.1800927.
[13]Radigan KA,Nicholson TT,Welch LC,et al.Influenza A Virus Infection Induces Muscle Wasting via IL-6 Regulation of the E3Ubiquitin Ligase Atrogin-1[J].J Immunol,2019,202(2)∶484-493.DOI∶10.4049/jimmunol.1701433.
[14]Ramos JM,Garcia-Navarro M,Moreno V,et al.Interleukin(IL)-1β,IL-6 and tumor necrosis factor in patients with seasonal flu[J].Rev Esp Quimioter,2018,31(6)∶542-545.
[15]孙子梅.血清细胞因子检测在儿童肺炎支原体肺炎诊治中的意义[J].海南医学院学报,2016,22(3)∶273-275.DOI∶10.13210/j.enki.jhmu.20151030.01.
[16]Patel JA,Nair S,Ochoa EE,et a1.Interleukin-6-174 and tumor necrosis factorɑ-308 polymorphisms enhance cytokine production by human macrophages exposed torespiratory viruses[J].Interferon Cytokine Res,2010,30(12)∶917-921.DOI∶10.1089/jir.2010.0033.
[17]郑晶晶,顾玉海.低氧条件下IL-6、IL-8、IL-10作用机制研究进展[J].国际呼吸杂志,2016,36(3)∶224-227.DOI∶10.3760/cma.j.issn.1673-436X.2016.03.014.
[18]Chang WJ,Du Y,Zhao X,et al.Inflammation-related factors predicting prognosis of gastric cancer[J].World J Gastroenterol,2014,20(16)∶4586-4596.DOI∶10.3748/wjg.v20.i16.4586.
[19]Cai M,Zhang X,Li Y,et al.Toll-like receptor3 activation drives the inflammatory response in oxygen-induced retinopathy in rats[J].Br J Ophthalmol,2015,99(1)∶125-132.DOI∶10.1136/bjophthalmol-2014-305690.
[20]宋振举,童朝阳.严重脓毒症免疫调节治疗∶从免疫抑制走向免疫增强[J].中华急诊医学杂志,2014,23(4)∶365-368.DOI∶10.3760/cma.j.issn.1671-0282.2014.04.001.
[21]温前宽,李彦,杨建萍,等.严重脓毒症患者炎症因子的动态变化及预后意义[J].中华急诊医学杂志,2015,24(7)∶779-783.DOI∶10.3760/cma.j.issn.1671-0282.2015.07.020.