Division of Pathway Medicine, University of Edinburgh, Edinburgh, UK.
Curr Opin Infect Dis. 2013 Jun;26(3):213-8. doi: 10.1097/QCO.0b013e32835fb8bf.
Sepsis is a serious complication in preterm and term infants, yet our understanding of how neonates respond to infection remains poorly defined.
We describe our current clinical, cellular and molecular understanding of the neonatal host systemic response to infection. We find that host resilience essentially relies on innate immune mechanisms despite there being a complete repertoire of cellular components of the adaptive immune arm. The functional interplay between metabolism, immunity and microbiome further suggests that neonatal vulnerability to infection is not simply due to immaturity of the immune system but how immune homeostasis is regulated. Further research is required for exploring regulatory homeostatic mechanisms between innate and adaptive responses and microbiome colonization at birth, but which can impart an adverse trajectory to infection.
The vulnerability and resilience against infection in neonates, including extreme preterm infants, still remains poorly understood. We advance the view that greater consideration should be given to understanding the set point in the regulation of homeostatic control of innate and adaptive immunity and its interplay with metabolism and the newly acquired microbiome.
败血症是早产儿和足月儿的严重并发症，但我们对新生儿如何对感染做出反应的理解仍不清楚。
我们描述了目前对新生儿宿主对感染的全身反应的临床、细胞和分子理解。我们发现，尽管适应性免疫臂有完整的细胞成分库，但宿主的恢复力主要依赖于先天免疫机制。代谢、免疫和微生物组之间的功能相互作用进一步表明，新生儿对感染的易感性不仅仅是由于免疫系统不成熟，而是免疫稳态是如何调节的。需要进一步研究探索先天和适应性反应以及出生时微生物组定植之间的调节性稳态机制，但这可能会对感染产生不利影响。
新生儿（包括极早产儿）对感染的易感性和抵抗力仍知之甚少。我们认为，应该更加重视理解先天和适应性免疫的稳态控制的调节设定点，以及它与代谢和新获得的微生物组的相互作用。
