Maltodextrin-induced intestinal injury in a neonatal mouse model

Autor: Yan Liu, Camilia R. Martin, Pratibha Singh, George Perides, David Ramiro-Cortijo, Lady Leidy Sanchez-Fernandez, William Yakah, Esli Medina-Morales, Pedro Ochoa-Allemant, Steven D. Freedman
Rok vydání: 2020
Předmět:
0301 basic medicine
Klebsiella pneumoniae
lcsh:Medicine
Medicine (miscellaneous)
Neonatal mouse model
Pathogenesis
0302 clinical medicine
Immunology and Microbiology (miscellaneous)
Necrotizing enterocolitis
Intestine
Small
Intestinal Mucosa
Hypoxia
Microvilli
biology
Tight junction
Cytokines
Goblet Cells
Inflammation Mediators
medicine.symptom
lcsh:RB1-214
Research Article
medicine.medical_specialty
Programmed cell death
Neuroscience (miscellaneous)
Permeability
General Biochemistry
Genetics and Molecular Biology
03 medical and health sciences
Maltodextrin
Enterocolitis
Necrotizing
Polysaccharides
030225 pediatrics
Internal medicine
lcsh:Pathology
medicine
Animals
Mucin-2
Tight Junction Proteins
Intestinal permeability
business.industry
lcsh:R
Hypoxia (medical)
biology.organism_classification
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Endocrinology
Animals
Newborn
Infant formula
Intestinal injury
business
Zdroj: Disease Models & Mechanisms
article-version (VoR) Version of Record
Disease Models & Mechanisms, Vol 13, Iss 8 (2020)
ISSN: 1754-8411
1754-8403
DOI: 10.1242/dmm.044776
Popis: Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of this study was to test in neonatal mice the effect of maltodextrin, a complex carbohydrate, on the risk of intestinal injury. The goal was to develop a robust and highly reproducible murine model of intestinal injury that allows insight into the pathogenesis and therapeutic interventions of nutrient-driven intestinal injury. Five- to 6-day-old C57BL/6 mice were assigned to the following groups: dam fed (D); D+hypoxia+Klebsiella pneumoniae; maltodextrin-dominant human infant formula (M) only; M+hypoxia; and M+hypoxia+K. pneumoniae. The mice in all M groups were gavage fed five times a day for 4 days. Mice were exposed to hypoxia twice a day for 10 min prior to the first and last feedings, and K. pneumoniae was added to feedings as per group assignment. Mice in all M groups demonstrated reduced body weight, increased small intestinal dilatation and increased intestinal injury scores. Maltodextrin-dominant infant formula with hypoxia led to intestinal injury in neonatal mice accompanied by loss of villi, increased MUC2 production, altered expression of tight junction proteins, enhanced intestinal permeability, increased cell death and higher levels of intestinal inflammatory mediators. This robust and highly reproducible model allows for further interrogation of the effects of nutrients on pathogenic factors leading to intestinal injury and NEC in preterm infants. This article has an associated First Person interview with the first author of the paper.
Summary: Using maltodextrin-dominant human infant formula feeding in combination with hypoxia, we developed a highly reproducible model of small intestinal injury in the neonatal mouse.
Databáze: OpenAIRE
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