Source:http://linkedlifedata.com/resource/pubmed/id/17991705
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2008-1-18
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| pubmed:abstractText |
Loss of intestinal epithelial barrier function (EBF) is a major problem associated with total parenteral nutrition (TPN) administration. We have previously identified intestinal intraepithelial lymphocyte (IEL)-derived interferon-gamma (IFN-gamma) as a contributing factor to this barrier loss. The objective was to determine whether other IEL-derived cytokines may also contribute to intestinal epithelial barrier breakdown. C57BL6J male mice received TPN or enteral nutrition (control) for 7 days. IEL-derived interleukin-10 (IL-10) was then measured. A significant decline in IEL-derived IL-10 expression was seen with TPN administration, a cytokine that has been shown in vitro to maintain tight junction integrity. We hypothesized that this change in IEL-derived IL-10 expression could contribute to TPN-associated barrier loss. An additional group of mice was given exogenous recombinant IL-10. Ussing chamber experiments showed that EBF markedly declined in the TPN group. TPN resulted in a significant decrease of IEL-derived IL-10 expression. The expression of several tight junction molecules also decreased with TPN administration. Exogenous IL-10 administration in TPN mice significantly attenuated the TPN-associated decline in zonula occludens (ZO)-1, E-cadherin, and occludin expression, as well as a loss of intestinal barrier function. TPN administration led to a marked decline in IEL-derived IL-10 expression. This decline was coincident with a loss of intestinal EBF. As the decline was partially attenuated with the administration of exogenous IL-10, our findings suggest that loss of IL-10 may be a contributing mechanism to TPN-associated epithelial barrier loss.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Cldn2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/F11r protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/claudin 15,
http://linkedlifedata.com/resource/pubmed/chemical/claudin 7, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/occludin,
http://linkedlifedata.com/resource/pubmed/chemical/zonula occludens-1 protein
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jan
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| pubmed:issn |
0193-1857
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
294
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
G139-47
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| pubmed:meshHeading |
pubmed-meshheading:17991705-Animals,
pubmed-meshheading:17991705-Bacterial Translocation,
pubmed-meshheading:17991705-Cadherins,
pubmed-meshheading:17991705-Cell Adhesion Molecules,
pubmed-meshheading:17991705-Down-Regulation,
pubmed-meshheading:17991705-Electric Impedance,
pubmed-meshheading:17991705-Interleukin-10,
pubmed-meshheading:17991705-Intestinal Absorption,
pubmed-meshheading:17991705-Intestinal Mucosa,
pubmed-meshheading:17991705-Male,
pubmed-meshheading:17991705-Membrane Proteins,
pubmed-meshheading:17991705-Mice,
pubmed-meshheading:17991705-Mice, Inbred C57BL,
pubmed-meshheading:17991705-Models, Animal,
pubmed-meshheading:17991705-Parenteral Nutrition, Total,
pubmed-meshheading:17991705-Permeability,
pubmed-meshheading:17991705-Phosphoproteins,
pubmed-meshheading:17991705-Receptors, Cell Surface,
pubmed-meshheading:17991705-Recombinant Proteins,
pubmed-meshheading:17991705-Tight Junctions
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| pubmed:year |
2008
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| pubmed:articleTitle |
Decline in intestinal mucosal IL-10 expression and decreased intestinal barrier function in a mouse model of total parenteral nutrition.
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| pubmed:affiliation |
Department of Surgery, University of Michigan Medical School, Ann Arbor, MI 48109-0245, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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