Abstract

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease that affects premature neonates. It frequently results in significant morbidity and mortality for those affected. Years of research into the pathophysiology of NEC have revealed it to be a variable and multifactorial disease. However, there are risk factors associated with NEC including low birth weight, prematurity, intestinal immaturity, alterations in microbial colonization, and history of rapid or formula based enteral feeds (Fig. 1).1–3 An accepted generalization of the pathogenesis of NEC includes a hyperresponsive immune reaction to insults such as ischemia, starting formula feeds, or alterations in the microbiome with pathologic bacterial colonization and translocation. This reaction causes a hyperinflammatory response disrupting the normal intestinal barrier, allowing abnormal bacterial translocation and ultimately sepsis.1,2,4 This review will focus specifically on the interactions with the microbiome and intestinal barrier function in NEC.

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