title: Early life response to infection.
abstract: OBJECTIVE
  Sepsis is a serious complication in preterm and term infants, yet our understanding of how neonates respond to infection remains poorly defined.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors: Division of Pathway Medicine, University of Edinburgh, Edinburgh, UK. p.ghazal@ed.ac.uk
authors: Peter
authors: P
authors: Ghazal
authors: Paul
authors: P
authors: Dickinson
authors: Claire L
authors: CL
authors: Smith
mesh_terms: D056704:Adaptive Immunity / Q000502:physiology*; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology; D007113:Immunity, Innate / Q000502:physiology*; D007231:Infant, Newborn; D007234:Infant, Premature / Q000276:immunology; D054892:Metagenome / Q000276:immunology; D018805:Sepsis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology