河北医科大学学报 ›› 2023, Vol. 44 ›› Issue (3): 305-309.doi: 10.3969/j.issn.1007-3205.2023.03.012

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IL-17/IL-23炎症轴在新生儿缺氧缺血性脑病发病中的作用机制探究

  

  1. 1.四川省绵阳市人民医院儿科,四川 绵阳 621000;2.四川省攀枝花市中心医院儿科,四川 攀枝花 617000

  • 出版日期:2023-03-25 发布日期:2023-03-24
  • 作者简介:邹良(1985-),女,四川绵阳人,四川省绵阳市人民医院主治医师,医学学士,从事儿科疾病诊治研究。
  • 基金资助:
    四川省医学(青年创新)科研课题(S20026)

The mechanism of IL-17/IL-23 inflammatory axis in the pathogenesis of neonatal hypoxic-ischemic encephalopathy

  1. 1.Department of Pediatrics, Mianyang People′s Hospital, Sichuan Province, Mianyang 621000, China; 
    2.Department of Pediatrics, Central Hospital of Panzhihua City, Sichuan Province, Panzhihua 617000, China
  • Online:2023-03-25 Published:2023-03-24

摘要: 目的 探究白细胞介素17(interleukin-17,IL-17)/白细胞介素23(interleukin-23,IL-23)炎症轴在新生儿缺氧缺血性脑病(hypoxic-ischemic encephalopathy,HIE)发病中的作用机制。
方法 选取四川省绵阳市人民医院HIE患儿90例作为研究组,另选足月正常新生儿90例作为对照组,比较2组一般资料(性别、胎龄、日龄、出生体重、分娩方式)、血清IL-17、IL-23水平,并比较研究组不同病情程度患儿血清IL-17、IL-23水平,采用Spearman相关系数模型分析血清IL-17、IL-23水平与HIE患儿病情程度的相关性,并采用新生儿神经行为(neonatal behavioral neurological assessment,NBNA)评估研究组患儿是否发生神经功能损伤,比较发生与未发生神经功能损伤患儿血清IL-17、IL-23水平,采用受试者工作特征(receiver operating characteristic,ROC)曲线分析血清IL-17、IL-23水平诊断HIE患儿神经功能损伤的价值。
结果 研究组血清IL-17、IL-23水平均高于对照组(P<0.05);重度患儿血清IL-17、IL-23水平高于中度患儿、轻度患儿,中度患儿血清IL-17、IL-23水平高于轻度患儿(P<0.05);血清IL-17、IL-23水平与HIE患儿病情程度呈正相关(r=0.826、0.845,P<0.05);发生神经功能损伤患儿血清IL-17、IL-23水平均高于未发生神经功能损伤患儿(P<0.05);血清IL-17、IL-23水平单独诊断HIE患儿发生神经功能损伤的曲线下面积(area under the curve,AUC)分别为0.829(95%CI:0.735~0.900)、0.744(95%CI:0.641~0.830),二者联合诊断的AUC为0.934(95%CI:0.641~0.830),诊断敏感度、特异度分别为92.31%、90.62%。
结论 HIE患儿IL-17/IL-23炎症轴被激活,血清IL-17、IL-23水平升高,可促进HIE患儿病情程度加重,导致神经功能损伤。


关键词: 缺氧缺血,脑, 婴儿,新生, 白细胞介素17

Abstract: Objective To explore the mechanism of interleukin-17 (IL-17)/interleukin-23 (IL-23) inflammatory axis in the pathogenesis of neonatal hypoxic-ischemic encephalopathy (HIE). 
Methods We selected 90 children with HIE from Mianyang People′s Hospital, Sichuan Province, as the research group, and another 90 full-term normal newborns as the control group. The general data (sex, gestational age, age, birth weight, delivery mode), and serum IL-17 and IL-23 levels of the two groups were compared, and the serum IL-17 and IL-23 levels of children with different disease severity in the research group were compared. Spearman correlation coefficient model was used to analyze the correlation between the serum levels of IL-17 and IL-23 and the disease severity of children with HIE. Neonatal behavioral neurological assessment (NBNA) was used to assess whether the children in the research group suffered from neurological impairment, and the levels of IL-17 and IL-23 in the serum of children with and without neurological impairment were compared. The receiver operating characteristic (ROC) curve was used to analyze the value of the serum levels of IL-17 and IL-23 in the diagnosis of neurological impairment in children with HIE. 
Results The serum levels of IL-17 and IL-23 in the research group were higher than those in the control group (P<0.05). The serum levels of IL-17 and IL-23 in severe HIE children were higher than those in moderate and mild HIE children, and higher in moderate HIE children than in mild HIE children (P<0.05). The serum levels of IL-17 and IL-23 were positively correlated with the severity of HIE (r=0.826, 0.845, P<0.05). The serum levels of IL-17 and IL-23 in children with neurological impairment were higher than those in children without neurological impairment (P<0.05). The area under the ROC curve (AUC) of serum IL-17 and IL-23 levels for the diagnosis of neurological impairment in HIE children was 0.829 (95%CI: 0.735-0.900) and 0.744 (95%CI: 0.641-0.830), respectively. The AUC of combined diagnosis of the two levels was 0.934 (95%CI: 0.641-0.830), and the diagnostic sensitivity and specificity were 92.31% and 90.62%, respectively. 
Conclusion The IL-17/IL-23 inflammatory axis is activated in children with HIE, and the serum levels of IL-17 and IL-23 increase, which can promote the aggravation of the disease in children with HIE and lead to neurological impairment. 


Key words: hypoxia-ischemia, brain, infant, newborn, interleukin-17