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

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Willems, R, Krych, L, Rybicki, V, Jiang, P, Sangild, PT, Shen, RL, Hensel, KO, Wirth, S, Postberg, J & Jenke, AC 2015, 'Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs' Epigenomics, bind 7, nr. 4, s. 553-65. https://doi.org/10.2217/epi.15.13

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Willems, Rhea ; Krych, Lukasz ; Rybicki, Verena ; Jiang, Pingping ; Sangild, Per T ; Shen, René L ; Hensel, Kai O ; Wirth, Stefan ; Postberg, Jan ; Jenke, Andreas C. / Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs. I: Epigenomics. 2015 ; Bind 7, Nr. 4. s. 553-65.

Bibtex

@article{aab33981a6254a5bb3903863b43ac7b4,
title = "Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs",
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.",
author = "Rhea Willems and Lukasz Krych and Verena Rybicki and Pingping Jiang and Sangild, {Per T} and Shen, {Ren{\'e} L} and Hensel, {Kai O} and Stefan Wirth and Jan Postberg and Jenke, {Andreas C}",
year = "2015",
doi = "10.2217/epi.15.13",
language = "English",
volume = "7",
pages = "553--65",
journal = "Epigenomics",
issn = "1750-1911",
publisher = "Future Medicine Ltd",
number = "4",

}

RIS

TY - JOUR

T1 - Introducing enteral feeding induces intestinal subclinical inflammation and respective chromatin changes in preterm pigs

AU - Willems, Rhea

AU - Krych, Lukasz

AU - Rybicki, Verena

AU - Jiang, Pingping

AU - Sangild, Per T

AU - Shen, René L

AU - Hensel, Kai O

AU - Wirth, Stefan

AU - Postberg, Jan

AU - Jenke, Andreas C

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

U2 - 10.2217/epi.15.13

DO - 10.2217/epi.15.13

M3 - Journal article

VL - 7

SP - 553

EP - 565

JO - Epigenomics

JF - Epigenomics

SN - 1750-1911

IS - 4

ER -

ID: 46276801