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Updated: Apr 8, 2026
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
Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm
Rhea Willems1, Lukasz Krych2, Verena Rybicki1
1Department of Paediatrics, HELIOS Medical Centre Wuppertal, Centre for Clinical & Translational Research (CCTR), Faculty of Health, Centre for Biomedical Education & Research (ZBAF), Witten/Herdecke University, Heusnerstr. 40,42283 Wuppertal, Germany.
Aim:
To analyze how enteral food introduction affects intestinal gene regulation and chromatin structure in preterm pigs.
Materials & Methods:
Preterm pigs were fed parenteral nutrition plus/minus slowly increasing volumes of enteral nutrition. Intestinal gene-expression and chromatin structure were analyzed 5 days after birth.
Results:
Enteral feeding led to differential upregulation of inflammatory and pattern recognition receptor genes, including IL8 (median: 5.8, 95% CI: 3.9-7.8 for formula; median: 2.2, 95% CI: 1.3-3.3 for colostrum) and TLR4 (median: 3.7, 95% CI: 2.6-4.8 for formula; no significant differences for colostrum) with corresponding decondensed chromatin configurations. On histology this correlated with mild mucosal lesions, particularly in formula-fed pigs. In CaCo-2 cells, histone hyperacetylation led to a marked increase in TLR4 mRNA and increased IL8 expression upon stimulation with lipopolysaccharide (median: 7.0; interquartile range: 5.63-8.85) compared with naive cells (median 4.2; interquartile range: 2.45-6.33; p = 0.03).
Conclusion:
Enteral feeding, particular with formula, induces subclinical inflammation in the premature intestine and more open chromatin structure in key inflammatory genes. This may increase the susceptibility for necrotizing enterocolitis.
