新生儿缺氧缺血性脑病血浆Th2源细胞因子水平的研究被引量：4

Study on Plasma Levels of Th2 Cytokines in Neonates with Hypoxic Ischemic Encephalopathy

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摘要目的　研究新生儿缺氧缺血性脑病 (HIE)患儿辅助性T淋巴细胞亚群 2 (Th2 )细胞功能变化及其与HIE间的关系。　方法　采用ELISA法和单克隆抗体间接免疫荧光法 ,检测 4 6例HIE患儿不同病期血浆和外周血单个核细胞 (PBMC)体外分别产生白细胞介素 (IL) 6、IL 8、IL 10水平和T细胞IL 2受体 (IL 2R)表达率 ,并与正常足月新生儿脐血 (2 0例 )进行对照。　结果　HIE病程第 1天血浆及PBMC体外产生IL 6 [分别为 6 6 .3、80 4 .5ng L(中位数 ,以下同 ) ]、IL 8(4 10 .5、1983.6ng L)和IL 10 (2 7.9、14 0 .1ng L) ,明显高于正常脐血对照组 (分别为 1.9、187.7;91.0、76 6 .8;2 .6、16 .4ng L) (Z =4 .6 5 3～ 5 .85 6 ,P <0 .0 1) ;中重度组及并发多器官功能损害 (MOD)的HIE患儿血浆及PBMC体外产生IL 6 (分别为 86 .0、12 36 .4 ;111.3、174 6 .9ng L)、IL 8(分别为5 79.5、2 812 .2 ;5 32 .8、2 94 3.3ng L) ,分别高于轻度组 (分别为 5 2 .6、5 83.4 ;335 .3、15 2 8.9ng L)及无MOD组 (分别为 5 6 .6、713.8;35 2 .4、15 72 .4ng L)患儿 (Z =2 .2 2 8～ 2 .70 1,P <0 .0 5 ;Z =2 .877～4 .187,P <0 .0 1) ,而IL 10差异无显著性 (Z =0 .4 5 0～ 1.85 0 ,P >0 .0 5 ) ;T细胞IL 2R表达率 [(5 2 .8± 13.4 ) % ]明显? Objective To study the change and inter-relationship of function of help-2 T lymphocyte (Th2) in neonates with hypoxic-ischemic encephalopathy (HIE). Methods Umbilical cord blood of 20 normal full-term infants serves as control. The levels of interleukin (IL)-6, IL-8 and IL-10 in plasma and supernatant of cultured peripheral blood mononuclear cells (PBMC), and expression rates of IL-2 receptor (IL-2R) on T cells were measured in 46 neonates with different stage HIE. Results Both plasma and supernatant of PBMC levels of IL-6(66.3 ng/L, 804.5 ng/L,median), IL-8(410.5 ng/L, 1983.6 ng/L) and IL-10 (27.9 ng/L, 140.1 ng/L) in the first day (D1) in HIE infants were much higher than control(1.9 ng/L, 187.7 ng/L; 91.0 ng/L, 766.8 ng/L; and 2.6 ng/L,16.4 ng/L repectively).Z=4.653～5.856, P<0.01. Levels of IL-6(86.0 ng/L, 1236.4 ng/L; 111.3 ng/L, 1 746.9 ng/L)and IL-8 (579.5 ng/L, 2 812.2 ng/L; 532.8 ng/L, 2 943.3 ng/L) in plasma and supernatant of PBMC were much higher in patients with moderate/severe HIE or HIE with multi-organ damage (MOD) compared with infants with mild HIE (52.6 ng/L, 583.4 ng/L; 335.3 ng/L, 1 528.9 ng/L; respectively) and HIE without MOD(56.6 ng/L, 713.8 ng/L; 352.4 ng/L, 1 572.4 ng/L; respectively), Z=2.228～2.701, P<0.05; Z=2.877～4.187, P<0.01. There was no significant difference between levels of IL-10 in different groups Z=0.450～1.850,P>0.05. The expression rate of IL-2R on T cells in D1 of HIE[(52.8±13.4)%] was markedly lower than control [(64.0±7.0)%], especially in moderate/severe HIE. Plasma levels of IL-6, IL-8 and IL-10 correlated positively to each other r=0.629～0.749. Levels of IL-6, IL-8 and IL-10 in plasma and levels of IL-6 and IL-8 in supernatant of PBMC in HIE infants were correlated positively to surme CPK-BB, r=0.489～0.691, and negatively to expression rates of IL-2R on T cells, r=-0.394～ -0.451, There were no significant difference between levels of IL-6, IL-8 and IL-10 both in plasma and supernatant of PBMC on D1 (56.6 ng/L, 888.7 ng/L;352.3 ng/L, 1 879.4 ng/L; 27.7 ng/L, 99.1 ng/L; respectively) and D3 (52.7 ng/L, 876.2 ng/L; 320.7 ng/L,1 904.8 ng/L; 21.2 ng/L,183.4 ng/L;respectively), Z=0.314～1.371,P>0.05. Plasma levels of IL-6(14.2 ng/L) and IL-8 (238.4 ng/L)on D7 (remission of any syndromes) were markedly lower than those on D1 and D3, Z=2.455, P<0.05; Z=2.725～3.856, P<0.01. Plasma levels of IL-10 on D7 (19.9 ng/L) were lower than those on D1 and D3, but there were no statistic significance, Z=1.437, 1.248, P>0.05. Conclusion The function of Th2 lymphocyte is disordered and might play an important role in the pathogenesis of HIE.

作者张秋业

机构地区青岛大学医学院附属医院儿科

出处《中华围产医学杂志》 CAS 2003年第5期280-285,共6页 Chinese Journal of Perinatal Medicine

关键词新生儿缺氧缺血性脑病血浆 TH2细胞细胞因子 T淋巴细胞亚群2 Hypoxia-ischemia, brain Tha cells Interleukin-6 Interleukin-8 Interleukin-10 Infant, newborn

分类号 R722.1 [医药卫生—儿科]

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1史金阳,韩玉昆,孙桂莲,高红.新生大鼠缺氧缺血性脑损伤与肿瘤坏死因子基因表达的研究[J].中华儿科杂志,1999,37(2):87-89. 被引量：14
2刘晓红,黄静宁,刘皖君.新生儿缺氧缺血性脑病脑脊液和血浆IL-6水平的变化及临床意义[J].中华儿科杂志,2000,38(1):35-37. 被引量：27
3Maeda Y, Matsumoto M, Hori O, et al. Hypoxia/reoxygenation-mediated induction of astroeyte interleukin-6 : a paracrine mechanism potentially enhancing neuron survival. J Exp Med,1994,180 : 2297-2308.
4Baggiolini M, Walz A, Kunkel SL. Neutrophil-activating peptide-1/interleukin-8, a novel cytokine that activates neutrophils. J Clin Invest, 1989,84:1045-1049.
5Huber AR, Kunkel SL, Todd RF 3rd, et al. Regulation of transendothelial neutrophil migration by endogenous interleukin-8. Science, 1991,254 : 99-102.
6Eppihimer MJ, Granger DN. Ischemia/reperfusion-induced leukocyte-endothelial interactions in postcapillary venules. Shock,1997,8:16-25.
7Goldman M,Velu T. Interleukin-10 and its implications for immunopathology. Adv Nephrol, 1995,24 : 79-90.
8Seekamp A, Jochum M, Ziegler M, et al. Cytokines and adhesion molecules in eletive and accidental trauma-related ischemia/reperfusion. J Trauma,1998,44:874-882.
9Vora M, Romero LI, Karasek MA. Interleukin-10 induces Eselectin on small and large blood vessel endothelial cells. J Exp Med, 1996,184: 821-829.
10Szaflarski J, Burtrum D, Siverstein FS. Cerebral hypoxia-ischemia stimulate cytokines gene expression in perinatal rats.Stroke, 1995,26 : 1093-1110.