Diet-dependent mucosal colonization and interleukin-1beta responses in preterm pigs susceptible to necrotizing enterocolitis.

Objectives: Intestinal colonization challenges the neonatal innate immune system, especially in newborns with an immature immune response lacking the supportive bioactive components from mother's milk. Accordingly, formula-fed preterm pigs frequently show bacterial overgrowth, mucosal atrophy, and gut lesions reflecting necrotizing enterocolitis (NEC) within the first days after birth. We hypothesized that NEC development is related to a diet-dependent bacterial adherence and a subsequent proinflammatory cytokine response in the gut mucosa immediately after introduction of enteral food.

Temporal proteomic analysis of intestine developing necrotizing enterocolitis following enteral formula feeding to preterm pigs.

Necrotizing enterocolitis (NEC), a serious gastrointestinal inflammatory disease, frequently occurs in preterm neonates that fail to adapt to enteral nutrition. A temporal gel-based proteomics study was performed on porcine intestine with NEC lesions induced by enteral formula feeding. Functional assignment of the differentially expressed proteins revealed that important cellular functions, such as the heat shock response, protein processing; and purine, nitrogen, energy metabolism, were possible involved in the early progression of NEC.

The small intestine proteome is changed in preterm pigs developing necrotizing enterocolitis in response to formula feeding.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in newborn premature infants. Clinical studies show increased incidence of NEC in premature infants with enteral formula feeding; however, pathogenesis remains unclear. To identify the NEC-related proteins for molecular mechanisms, we applied proteomics analysis to characterize changes in the protein expression profile of newborn premature piglet intestines with NEC developed after enteral formula feeding for 24 h.