Perinatal inflammation influences but does not arrest rapid immune development in preterm babies

Infection and infection-related complications are important causes of death and morbidity following preterm birth. Despite this risk, there is limited understanding of the development of the immune system in those born prematurely, and of how this development is influenced by perinatal factors. Here we prospectively and longitudinally follow a cohort of babies born before 32 weeks of gestation. We demonstrate that preterm babies, including those born extremely prematurely (<28 weeks), are capable of rapidly acquiring some adult levels of immune functionality, in which immune maturation occurs independently of the developing heterogeneous microbiome. By contrast, we observe a reduced percentage of CXCL8-producing T cells, but comparable levels of TNF-producing T cells, from babies exposed to in utero or postnatal infection, which precedes an unstable post-natal clinical course. These data show that rapid immune development is possible in preterm babies, but distinct identifiable differences in functionality may predict subsequent infection mediated outcomes

Neonatal mucosal immunology

Although largely deprived from exogenous stimuli in utero, the mucosal barriers of the neonate after birth are bombarded by environmental, nutritional, and microbial exposures. The microbiome is established concurrently with the developing immune system. The nature and timing of discrete interactions between these two factors underpins the long-term immune characteristics of these organs, and can set an individual on a trajectory towards or away from disease. Microbial exposures in the gastrointestinal and respiratory tracts are some of the key determinants of the overall immune tone at these mucosal barriers and represent a leading target for future intervention strategies. In this review, we discuss immune maturation in the gut and lung and how microbes have a central role in this process

How nutrition and the maternal microbiota shape the neonatal immune system.

The mucosal surfaces of mammals are densely colonized with microorganisms that are commonly referred to as the commensal microbiota. It is believed that the fetus in utero is sterile and that colonization with microorganisms starts only after birth. Nevertheless, the unborn fetus is exposed to a multitude of metabolites that originate from the commensal microbiota of the mother that reach systemic sites of the maternal body. The intestinal microbiota is strongly personalized and influenced by environmental factors, including nutrition. Members of the maternal microbiota can metabolize dietary components, pharmaceuticals and toxins, which can subsequently be passed to the developing fetus or the breast-feeding neonate. In this Review, we discuss the complex interplay between nutrition, the maternal microbiota and ingested chemicals, and summarize their effects on immunity in the offspring