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Diet- and colonization-dependent intestinal dysfunction predisposes to necrotizing enterocolitis in preterm pigs

Sangild, PT; Siggers, RH; Schmidt, M; Elnif, J; Bjornvad, CR; Thymann, T; Grondahl, ML; Hansen, AK; Jensen, SK and Boye, M, et al. (2006) In Gastroenterology 130(6). p.1776-1792
Abstract
Background & Aims: Preterm birth and formula feeding are key risk factors associated with necrotizing enterocolitis (NEC) in infants, but little is known about intestinal conditions that predispose to disease. Thus, structural, functional, and microbiologic indices were used to investigate the etiology of spontaneous NEC development in preterm pigs. Methods : Piglets were delivered by cesarean section at 92% gestation, reared in infant incubators, and fed infant formula or colostrum every 3 hours (n = 120) until tissue collection at 1-2 days of age. Results: Clinical and histopathologic signs of NEC were observed in 57% of pigs fed FORMULA (26/46) and in 5% of pigs fed COLOSTRUM (2/38) (P <.05). Relative to COLOSTRUM, both healthy... (More)
Background & Aims: Preterm birth and formula feeding are key risk factors associated with necrotizing enterocolitis (NEC) in infants, but little is known about intestinal conditions that predispose to disease. Thus, structural, functional, and microbiologic indices were used to investigate the etiology of spontaneous NEC development in preterm pigs. Methods : Piglets were delivered by cesarean section at 92% gestation, reared in infant incubators, and fed infant formula or colostrum every 3 hours (n = 120) until tissue collection at 1-2 days of age. Results: Clinical and histopathologic signs of NEC were observed in 57% of pigs fed FORMULA (26/46) and in 5% of pigs fed COLOSTRUM (2/38) (P <.05). Relative to COLOSTRUM, both healthy and sick FORMULA pigs had reduced intestinal villous heights, enzyme activities, nutrient absorption, and antioxidant levels and higher inducible nitric oxide synthetase activity (P <.05). In healthy pigs, mucosal microbial diversity remained low and diet independent. NEC pigs showed bacterial over-growth, and a high mucosal density of Clostridium perfringens was detected in some but not all pigs. Germfree conditions and antiserum against Clostridium perfringens toxin prevented intestinal dysfunction and NEC in formula-fed pigs, whereas the gut trophic factors, epidermal growth factor, and glucagon-like peptide 2 had limited effects. Conclusions: A subclinical, formula-induced mucosal atrophy and dysfunction predispose to NEC and bacterial overgrowth. The adverse feeding effects are colonization dependent and may be reduced by factors in colostrum that include antibodies against aggressive toxins such as those of Clostridium perfringens. (Less)
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Contribution to journal
publication status
published
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Gastroenterology
volume
130
issue
6
pages
1776 - 1792
publisher
W B Saunders
external identifiers
  • wos:000237686700028
  • pmid:16697741
  • scopus:33646356953
ISSN
1528-0012
DOI
10.1053/j.gastro.2006.02.026
language
English
LU publication?
yes
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331ab215-8709-48b4-b2f9-1f521ceddfee (old id 408661)
date added to LUP
2007-10-17 19:06:47
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2019-08-14 01:39:49
@article{331ab215-8709-48b4-b2f9-1f521ceddfee,
  abstract     = {Background &amp; Aims: Preterm birth and formula feeding are key risk factors associated with necrotizing enterocolitis (NEC) in infants, but little is known about intestinal conditions that predispose to disease. Thus, structural, functional, and microbiologic indices were used to investigate the etiology of spontaneous NEC development in preterm pigs. Methods : Piglets were delivered by cesarean section at 92% gestation, reared in infant incubators, and fed infant formula or colostrum every 3 hours (n = 120) until tissue collection at 1-2 days of age. Results: Clinical and histopathologic signs of NEC were observed in 57% of pigs fed FORMULA (26/46) and in 5% of pigs fed COLOSTRUM (2/38) (P &lt;.05). Relative to COLOSTRUM, both healthy and sick FORMULA pigs had reduced intestinal villous heights, enzyme activities, nutrient absorption, and antioxidant levels and higher inducible nitric oxide synthetase activity (P &lt;.05). In healthy pigs, mucosal microbial diversity remained low and diet independent. NEC pigs showed bacterial over-growth, and a high mucosal density of Clostridium perfringens was detected in some but not all pigs. Germfree conditions and antiserum against Clostridium perfringens toxin prevented intestinal dysfunction and NEC in formula-fed pigs, whereas the gut trophic factors, epidermal growth factor, and glucagon-like peptide 2 had limited effects. Conclusions: A subclinical, formula-induced mucosal atrophy and dysfunction predispose to NEC and bacterial overgrowth. The adverse feeding effects are colonization dependent and may be reduced by factors in colostrum that include antibodies against aggressive toxins such as those of Clostridium perfringens.},
  author       = {Sangild, PT and Siggers, RH and Schmidt, M and Elnif, J and Bjornvad, CR and Thymann, T and Grondahl, ML and Hansen, AK and Jensen, SK and Boye, M and Moelbak, L and Buddington, RK and Weström, Björn and Holst, JJ and Burrin, DG},
  issn         = {1528-0012},
  language     = {eng},
  number       = {6},
  pages        = {1776--1792},
  publisher    = {W B Saunders},
  series       = {Gastroenterology},
  title        = {Diet- and colonization-dependent intestinal dysfunction predisposes to necrotizing enterocolitis in preterm pigs},
  url          = {http://dx.doi.org/10.1053/j.gastro.2006.02.026},
  volume       = {130},
  year         = {2006},
}