Abstract
The pathogenesis of necrotizing enterocolitis (NEC) is complex and its speed of progression is variable. To gain understanding of the disease, researchers have examined tissues resected from patients with NEC; however, as these are obtained at late stages of the disease, they do not yield clues about the early pathogenic events leading to NEC. Therefore, animal models are used and have helped identify a role for several mediators of the inflammatory network in NEC. In this article, we discuss the evidence for the role of these inflammatory mediators and conclude with a current unifying hypothesis regarding NEC pathogenesis.
