The
role of gut
microbiota,
along with the corresponding translocation of endotoxin into circulation, has
been demonstrated for many diseases including Crohn's Disease, ulcerative
colitis, HIV and diabetes. A recent publication in the Journal of Clinical Gastroenterology has extended this to liver
disease. Using several different mouse models to simulate liver disease, they
found significant differences in the microbiome compared to healthy control
mice. Several mechanisms for this link were explored, including an increase in
gut permeability leading to an increase in circulating endotoxin. Given that
Toll-like receptors are required for sensitivity to liver fibrosis, and the
role that endotoxin plays in other inflammatory diseases, this is an especially
attractive possibility.
Posted by Tim Sandle
Posted by Tim Sandle
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