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Date: | Thu, 18 May 2006 22:56:52 -0400 |
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<<Disclaimer: Verify this information before applying it to your situation.>>
I previously discussed how liver abnormalities are highly prevalent in
celiac disease. Why damage to the liver occurs is unknown, and gluten
toxicity and increased intestinal permeability have been proposed as
factors. The following free full text article appearing in the current
issue of Gastroenterolgy may shed light on why liver damage occurs in
celiacs.
Toll-like receptors (TLRs) reside on the surface of many cells which
participate in the immune system. TLRs sense molecules present in
pathogens but not the host, and when the immune system senses these
molecules, chemicals are released which set off inflammatory and
antipathogen responses. One class of molecules recognized by TLRs and
common to most pathogenic bacteria is lipopolysaccharides (LPS).
Gluten increases intestinal permeability in celiacs. The disuption of the
intestinal barrier permits endotoxins, such as LPS, from gut bacteria to
reach the portal vein of the liver triggering a TLR response from immune
cells in the liver. Proinflammatory mediators are released cascading into
the release of more chemicals leading to inflammation and liver damage.
This may be the cause of liver damage in celiacs. Gluten itself could
also trigger a liver immune response. Kupffer cells in the liver are
capable of antigen presentation to liver dendritic cells, and thus could
initiate a T cell response to gluten within the liver.
The following article is somewhat technical, but discusses the role of
various liver cells involved in the immune process and how intestinal
permeability and TLRs contribute to liver injury. The article is a good
read and provides valuable information about the liver I have not seen
elsewhere.
Gastroenterology Volume 130, Issue 6, Pages 1886-1900 (May 2006)
Toll-Like Receptor Signaling in the Liver
Robert F. Schwabe, Ekihiro Seki, David A. Brenner
Free Full Text:
http://www.gastrojournal.org/article/PIIS0016508506000655/fulltext
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