Prematurity is the leading cause of neonatal morbidity and mortality worldwide. Premature infants often require extended hospital stays, with increased risk of developing infection compared with term infants. A picture is emerging of wide-ranging deleterious consequences resulting from innate immune system activation in the newborn infant. Those who survive infection have been exposed to a stimulus that can impose long-lasting alterations into later life. In this review, we discuss sepsis-driven alterations in integrated neuroendocrine and metabolic pathways and highlight current knowledge gaps in respect of neonatal sepsis. We review established biomarkers for sepsis and extend the discussion to examine emerging findings from human and animal models of neonatal sepsis that propose novel biomarkers for early identification of sepsis. Future research in this area is required to establish a greater understanding of the distinct neonatal signature of early and late-stage infection, to improve diagnosis, curtail inappropriate antibiotic use and promote precision medicine through a biomarker-guided empirical and adjunctive treatment approach for neonatal sepsis. There is an unmet clinical need to decrease sepsis-induced morbidity in neonates, to limit and prevent adverse consequences in later life and decrease mortality.

中文翻译：

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先天免疫激活对婴儿内分泌和代谢途径的影响

早产是全世界新生儿发病率和死亡率的主要原因。早产儿通常需要延长住院时间，与足月儿相比，发生感染的风险更高。新生儿先天免疫系统激活导致的广泛有害后果的图片正在出现。那些在感染中幸存下来的人已经接触到一种刺激，这种刺激可以对以后的生活造成持久的改变。在这篇综述中，我们讨论了脓毒症驱动的综合神经内分泌和代谢途径的改变，并强调了目前新生儿脓毒症方面的知识差距。我们回顾了已建立的脓毒症生物标志物，并扩展讨论以检查新生儿脓毒症人类和动物模型的新发现，这些发现提出了用于早期识别脓毒症的新型生物标志物。该领域的未来研究需要更好地了解新生儿早期和晚期感染的独特特征，通过生物标志物指导的新生儿败血症经验和辅助治疗方法改善诊断，减少抗生素的不当使用并促进精准医疗. 在降低新生儿败血症诱发的发病率、限制和预防晚年的不良后果以及降低死亡率方面存在未满足的临床需求。