Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Sun, X; Yang, H; Nose, K; Nose, S; Haxhija, EQ; Koga, H; Teitelbaum, DH.
Decline in intestinal mucosal IL-10 expression and decreased intestinal barrier function in a mouse model of total parenteral nutrition.
Am J Physiol Gastrointest Liver Physiol. 2008; 294(1):G139-G147
Doi: 10.1152/ajpgi.00386.2007
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- Co-Autor*innen der Med Uni Graz
- Haxhija Emir
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- Abstract:
- 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.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Bacterial Translocation -
- Cadherins - metabolism
- Cell Adhesion Molecules - metabolism
- Down-Regulation -
- Electric Impedance -
- Interleukin-10 - metabolism
- Intestinal Absorption -
- Intestinal Mucosa - metabolism
- Male -
- Membrane Proteins - metabolism
- Mice -
- Mice, Inbred C57BL -
- Models, Animal -
- Parenteral Nutrition, Total -
- Permeability -
- Phosphoproteins - metabolism
- Receptors, Cell Surface - metabolism
- Recombinant Proteins - metabolism
- Tight Junctions - metabolism
- Find related publications in this database (Keywords)
- tight junction
- epithelial barrier function
- adherens junctional molecule 1 (JAM-1)
- claudins