ABSTRACT
With rupture of the amniotic membranes and birth, the intestine becomes exposed to maternal and environmental bacteria that rapidly colonize the mucosal surface and proliferate to form an early enteric microbiota. This early microbiota exhibits low resilience and high individuality and thus contains varying concentrations of immunostimulatory microorganisms and microbial constituents. The transition from a fetal sterile body surface to a densely colonized mucosa tissue after birth and the host mechanisms that facilitate this process are only beginning to be understood. The emerging results indicate that a large array of both developmentally regulated and adaptive mechanisms of the mature neonatal immune system and breast milk control immune stimulation and ensure tissue homeostasis. In contrast, the immature mucosal immune system of the premature neonate appears to be less able to prevent an inappropriate immune stimulation. Early colonization of the premature neonate by highly immunostimulatory bacteria in combination with an immature immune system may thereby lead to overt inflammation, tissue destruction, and disease.
