Elevated serum IL-10 is associated with severity of neonatal encephalopathy and adverse early childhood outcomes.

Elevated serum IL-10 is associated with severity of neonatal encephalopathy and adverse early childhood outcomes.
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血清IL-10升高与新生儿脑病的严重程度和儿童早期不良结局有关。

DOI:
10.1038/s41390-021-01438-1
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发表时间:
2022-07
期刊:
影响因子:
3.6
通讯作者:
Tann, Cally J.
Tann, Cally J.
中科院分区:
医学3区
文献类型:
--
作者:
Pang, Raymand;Mujuni, Brian M.;Martinello, Kathryn A.;Webb, Emily L.;Nalwoga, Angela;Ssekyewa, Julius;Musoke, Margaret;Kurinczuk, Jennifer J.;Sewegaba, Margaret;Cowan, Frances M.;Cose, Stephen;Nakakeeto, Margaret;Elliott, Alison M.;Sebire, Neil J.;Klein, Nigel;Robertson, Nicola J.;Tann, Cally J.

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新生儿脑病(NE)对全球儿童死亡率和残疾有重大影响。我们比较了有和没有 NE、有和没有围产期感染或炎症的足月乌干达新生儿的细胞因子谱,并确定了预测新生儿和幼儿结局的生物标志物。在这项探索性生物标志物研究中,比较了有或没有围产期感染/炎症的 NE 和非 NE 婴儿的血清 IL-1α、IL-6、IL-8、IL-10、TNFα 和 VEGF(<12 小时)。对新生儿(NE 严重程度、死亡率)和幼儿期(死亡或神经发育障碍至 2.5 岁)的结局进行了评估。通过多变量线性和逻辑回归以及接受者操作特征分析来探索结果的预测因素。对 159 名 NE 婴儿和 157 名非 NE 婴儿进行了细胞因子测定;分别有 150 人和 129 人获得了有关幼儿期结局的数据。 NE 婴儿的 IL-10 (p<0.001)、IL-6 (p<0.017) 和 VEGF (p<0.001) 水平较低。与非 NE 婴儿相比,中度和重度 NE 与较​​高的 IL-10 水平相关 (p<<0.001)。 IL-1α 升高与围产期感染/炎症相关 (p = 0.013)。在 NE 婴儿中,IL-10 可以预测新生儿死亡率 (p = 0.01) 和儿童早期不良结局(调整后 OR 2.28,95% CI 1.35–3.86,p = 0.002)。我们的研究结果支持 IL-10 作为新生儿脑病后不良后果生物标志物的潜在作用。新生儿脑病是全球儿童死亡和残疾的常见原因。炎症细胞因子是脑病严重程度和结果的潜在生物标志物。在这个基于乌干达卫生机构的队列中,新生儿脑病与出生时血清 IL-10 和 IL-6 升高以及 VEGF 降低相关。出生后 12 小时内血清 IL-10 升高可预测新生儿脑病的严重程度、新生儿死亡率和儿童早期不良发育结局,与围产期感染或炎症无关,并为炎症过程的贡献提供证据。我们的研究结果支持 IL-10 作为撒哈拉以南非洲队列新生儿脑病后不良结局生物标志物的作用。
Neonatal encephalopathy (NE) contributes substantially to child mortality and disability globally. We compared cytokine profiles in term Ugandan neonates with and without NE, with and without perinatal infection or inflammation and identified biomarkers predicting neonatal and early childhood outcomes. In this exploratory biomarker study, serum IL-1α, IL-6, IL-8, IL-10, TNFα, and VEGF (<12 h) were compared between NE and non-NE infants with and without perinatal infection/inflammation. Neonatal (severity of NE, mortality) and early childhood (death or neurodevelopmental impairment to 2.5 years) outcomes were assessed. Predictors of outcomes were explored with multivariable linear and logistic regression and receiver-operating characteristic analyses. Cytokine assays on 159 NE and 157 non-NE infants were performed; data on early childhood outcomes were available for 150 and 129, respectively. NE infants had higher IL-10 (p < 0.001), higher IL-6 (p < 0.017), and lower VEGF (p < 0.001) levels. Moderate and severe NE was associated with higher IL-10 levels compared to non-NE infants (p < 0.001). Elevated IL-1α was associated with perinatal infection/inflammation (p = 0.013). Among NE infants, IL-10 predicted neonatal mortality (p = 0.01) and adverse early childhood outcome (adjusted OR 2.28, 95% CI 1.35–3.86, p = 0.002). Our findings support a potential role for IL-10 as a biomarker for adverse outcomes after neonatal encephalopathy. Neonatal encephalopathy is a common cause of child death and disability globally. Inflammatory cytokines are potential biomarkers of encephalopathy severity and outcome. In this Ugandan health facility-based cohort, neonatal encephalopathy was associated with elevated serum IL-10 and IL-6, and reduced VEGF at birth. Elevated serum IL-10 within 12 h after birth predicted severity of neonatal encephalopathy, neonatal mortality, and adverse early childhood developmental outcomes, independent of perinatal infection or inflammation, and provides evidence to the contribution of the inflammatory processes. Our findings support a role for IL-10 as a biomarker for adverse outcomes after neonatal encephalopathy in a sub-Saharan African cohort.
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