Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs

Epigenomics. 2015;7(4):553-65. doi: 10.2217/epi.15.13.

Abstract

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.

Keywords: DNA methylation; chromatin; enteral nutrition; necrotizing enterocolitis; premature infants.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Caco-2 Cells
  • Chromatin / genetics*
  • Enteral Nutrition / adverse effects*
  • Enterocolitis, Necrotizing / etiology
  • Enterocolitis, Necrotizing / genetics*
  • Enterocolitis, Necrotizing / therapy
  • Enterocolitis, Necrotizing / veterinary
  • Humans
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism
  • Swine
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism

Substances

  • Chromatin
  • Interleukin-8
  • Toll-Like Receptor 4