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Rigshospitalet - a part of Copenhagen University Hospital
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Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs

Research output: Contribution to journalJournal articleResearchpeer-review

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  1. Human adipogenesis is associated with genome-wide DNA methylation and gene-expression changes

    Research output: Contribution to journalJournal articleResearchpeer-review

  1. Prenatal inflammation suppresses blood Th1 polarization and gene clusters related to cellular energy metabolism in preterm newborns

    Research output: Contribution to journalJournal articleResearchpeer-review

  2. Gut and immune effects of bioactive milk factors in preterm pigs exposed to prenatal inflammation

    Research output: Contribution to journalJournal articleResearchpeer-review

  3. Pathogenesis and biomarkers for necrotizing enterocolitis: Getting any closer?

    Research output: Contribution to journalJournal articleResearchpeer-review

  • Rhea Willems
  • Lukasz Krych
  • Verena Rybicki
  • Pingping Jiang
  • Per T Sangild
  • René L Shen
  • Kai O Hensel
  • Stefan Wirth
  • Jan Postberg
  • Andreas C Jenke
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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.

Original languageEnglish
JournalEpigenomics
Volume7
Issue number4
Pages (from-to)553-65
Number of pages13
ISSN1750-1911
DOIs
Publication statusPublished - 2015

ID: 46276801