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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00097.2002
Submitted on March 13, 2002
Accepted on July 8, 2002
1 Department of Animal Sciences, University of Illinois, Urbana, IL, USA; Authors contributed equally., USA
2 Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA; Authors contributed equally., USA
3 Department of Food Science and Human Nutrition, University of Illinois, Urbana, IL, USA; Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA
4 Department of Animal Sciences, University of Illinois, Urbana, IL, USA; Department of Veterinary Pathobiology, University of Illinois, Urbana, IL, USA; Division of Nutritional Sciences, University of Illinois, Urbana, IL, USA
* To whom correspondence should be addressed. E-mail: hgaskins{at}uiuc.edu.
Total parenteral nutrition (TPN) impairs small intestine (SI) development and is associated with barrier failure, inflammation, and acidomucin goblet cell expansion in neonatal piglets. This study examined the relationship between intestinal goblet cell expansion and molecular and cellular indices of inflammation in neonatal piglets receiving TPN, 80% parenteral+20% enteral (PEN), or 100% enteral nutrition (TEN; control) for 3 or 7 days. Epithelial permeability, T-cell numbers, TNF-
and IFN-
mRNA expression, and epithelial proliferation and apoptosis were compared with goblet cell numbers over time. Epithelial permeability was similar to control in the TPN and PEN jejunum at d 3, but increased in the TPN jejunum by d 7. By d 3, intestinal T-cell numbers were increased in TPN, but not PEN piglets. However, goblet cell expansion was established by d 3 in both the TPN and PEN ileum. Neither TNF- nor IFN- mRNA expression in the TPN and PEN ileum correlated with goblet cell expansion. Thus, goblet cell expansion occurred independently of overt inflammation, but in association with parenteral feeding. These data support the hypothesis that goblet cell expansion represents an initial defense triggered by reduced epithelial renewal to prevent intestinal barrier failure.
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