Immune Status in Very Preterm Neonates
Immune Status in Very Preterm Neonates
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DOI：
10.1542/peds.2011-1579
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发表时间：
2012-04-01
期刊：
影响因子：
8
通讯作者：
Peebles, Donald
中科院分区：
文献类型：
--
作者：
Azizia, Mallika;Lloyd, Jillian;Peebles, Donald
目的：与足月出生的新生儿相比，早产儿患败血症的风险更高。我们调查了极早产儿出生时和早期新生儿的免疫状态及其与短期结局的关系。方法：在一所大学医院进行前瞻性观察研究，招募了113名早产儿(23-32周)和78名对照。检测脐血和脐血中单核细胞主要组织相容性复合体(MHC)II类分子的表达、血清和体外脂多糖刺激的6种细胞因子(肿瘤坏死因子a、白介素1β、白介素6、白介素8、白介素10和白介素12p70)水平。结果：早产(早产和早产胎膜早破)、新生儿败血症和组织学绒毛膜羊膜炎与单核细胞MHC-II类表达显著减少有关。有证据表明随后出现迁延性脓毒症的新生儿在出生时MHC-II类表达水平较低。在所有早产儿中，连续单核细胞MHC-II类表达在第2天开始下降，其程度受早产儿和败血症的影响，到第7天未完全恢复，提示早产儿胎膜早破和早产队列中存在免疫麻痹。全血脂多糖刺激试验显示，在随后发生败血症的早产儿中，肿瘤坏死因子α的值显著降低，表明有一定程度的免疫麻痹。结论：我们的数据支持这样的概念，即胎儿在早产前暴露于炎症中会导致随后的内毒素低反应(免疫麻痹)，从而增加随后的脓毒症和相关器官功能障碍的风险。儿科2012；129：e967-e974
OBJECTIVES: Preterm neonates are at increased risk of sepsis compared with those born at term. We investigated immune status at birth and early neonatal life in very preterm neonates and its association with short-term outcomes.METHODS: Prospective observational study conducted at a university hospital recruiting 113 preterm neonates (23-32 weeks) and 78 controls. Monocyte major histocompatibility complex (MHC) class II expression, serum, and ex vivo lipopolysaccharide stimulated levels of six cytokines (tumor necrosis factor a, interleukin (IL)-1 beta, IL-6, IL-8, IL-10, and IL-12p70) were measured in umbilical cord blood and over the first 7 days. The presence of neonatal sepsis and histologic chorioamnionitis was recorded.RESULTS: Prematurity (preterm labor and preterm premature rupture of membranes cohorts), neonatal sepsis, and histologic chorioamnionitis were associated with significant reduction in monocyte MHC class II expression. Neonates who had evidence of subsequent protracted sepsis had low levels of MHC class II expression at birth. Serial monocyte MHC class II expression revealed a fall by day 2, in all preterm neonates, with the degree being influenced by both prematurity and sepsis, and incomplete recovery by day 7, suggesting immunoparalysis in preterm premature rupture of membranes and preterm labor cohorts. Whole blood lipopolysaccharide stimulation assay showed significantly lower tumor necrosis factor a, values in preterm neonates who subsequently developed sepsis indicating a degree of immunoparalysis.CONCLUSIONS: Our data support the concept that fetal exposure to inflammation before preterm delivery leads to subsequent endotoxin hyporesponsiveness (immunoparalysis), which increases the risk of subsequent sepsis and associated organ dysfunction. Pediatrics 2012;129:e967-e974