The preterm intestine is not ready for life outside the womb because of its impaired digestive, absorptive, and motility capabilities. Intestinal barrier function is inadequate and enterocyte contributions to innate immunity are hyper-responsive, predisposing the infant to inflammatory disease and sepsis. Microbial colonization plays a significant role in normal postnatal development of the intestine. Microbial-host interactions can enhance motility, digestion, and absorption, in addition to strengthening barrier function and encouraging immune homeostasis. These benefits are not seen in preterm infants who experience delayed and altered microbial community colonization after birth, termed dysbiosis. In combination with the reduced gut functions in the preterm infant, dysbiosis can further damage existing gut functions and exacerbate the hyper-reactive inflammatory state, which increases the risk for inflammatory diseases such as necrotizing enterocolitis (NEC). This chapter details the role of the microbiome in intestinal maturation and outlines ways in which poor clinical outcomes in the preterm infant, such as NEC, could be circumvented through clinical interventions that optimize the microbiome community.
Humphrey, E., & Claud, E. (2018). Impact of Microbes on the Intestinal Development of the Preterm Infant. In Mechanisms Underlying Host-Microbiome Interactions in Pathophysiology of Human Diseases (pp. 1–33). Springer US. https://doi.org/10.1007/978-1-4939-7534-1_1