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Updated: May 14, 2026

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

Necrotizing enterocolitis and the placenta - a key etiological link.

Sam W Moore¹, Marion Arnold, Colleen Wright

¹Divisions of Pediatric Surgery, University of Stellenbosch, Tygerberg, Western Cape Tygerberg 7505, South Africa. swm@sun.ac.za

Journal of Pediatric Surgery

|February 19, 2013

Summary

Placental infections and vascular issues may predispose premature infants to necrotizing enterocolitis (NEC). This study found more placental pathology in infants with surgical NEC, suggesting antenatal infection plays a role.

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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

Published on: June 24, 2020

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Last Updated: May 14, 2026

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development

Published on: June 24, 2020

Area of Science:

Neonatal surgery
Perinatal pathology
Neonatal intensive care

Background:

Necrotizing enterocolitis (NEC) is a severe surgical condition in premature infants.
Antenatal factors like infections and vascular insufficiency may prime the inflammatory cascade for NEC.
Understanding placental pathology is crucial for NEC pathogenesis.

Purpose of the Study:

To investigate the association between placental pathology and the development of necrotizing enterocolitis (NEC).
To explore the role of placental factors in predisposing neonates to NEC.

Main Methods:

Evaluation of 5338 placentas from high-risk pregnancies for insufficiency, infarction, and infection.
Comparison of placental pathology in 72 infants with surgical NEC against unaffected infants.

Main Results:

Surgical NEC cases showed significantly higher rates of vascular pathology (placental infarcts) compared to high-risk controls (54.5% vs. 21%).
Placental infection/chorioamnionitis and villitis with fetal inflammatory response were more prevalent in surgical NEC infants (31.8% vs. 12%).

Conclusions:

Antenatal placental infection may contribute to NEC pathogenesis.
Placental infection might modify fetal vascular response, increasing NEC risk.
Further research is warranted to confirm the role of antenatal placental factors in NEC.