Ethanol Induced In Mice Liver

Liver 'kills immune cells'

Scientists say they have discovered that the liver can kill immune cells, a finding that they believe could pave the way for new approaches to graft rejection, and the fight against hepatitis and other chronic liver diseases.

An international team led by the University of Sydney, says he first observed in mice how the liver is independent, engulfing and destroying the body's defense forces-T-cells.

"In 2004, we discovered that healthy cells can overwhelm the liver active immune cells called T cells and now we have seen that the` T-cells are actually destroyed, "Dr. Patrick

Bertolino, who led the team said.

He added: "The liver is an amazing organ. Most people think it's just lower case of alcohol, but it` s plant of the body - breaking down substances that we don `t want and by those we do.

"We now know the liver cells are also able to subvert the order of the immune system.Our finding may explain why liver transplants have rejection rates lower than other organ transplants. "

In their research, scientists have found evidence of the healthy liver cells of mice eating the T cells, which was unexpected that this "cell cannibalism" had yet been seen in tumor cells.

A potential advantage of the research is to reduce the rejection of organ transplants, scientists say.

In transplants, the new body is seen by the body as a foreign object: the spleen or lymph nodes called naive T cells to reproduce and become killer T cells, which are sent out to invade and kill " foreign "cells.

What scientists have discovered the liver is going around the process - the liver cells signal to naive T cells and digest them before they have a chance to become killer T cells.

"Adenosine signaling contributes to ethanol-induced fatty liver in ...

Summary

Hepatic steatosis is frequently associated with alcohol ingestion and abuse. While the molecular pathogenesis of fatty change is well understood, biochemical and pharmacological mechanisms including ethanol stimulates these molecular changes remains unknown. During metabolism of ethanol, adenosine is generated by the enzyme ecto-5'-nucleotidase, and the production of adenosine and activation of the adenosine receptor are known to play a crucial role in the development of hepatic fibrosis. We therefore investigated whether adenosine and its receptors play a role in the development of alcohol-induced fatty liver.WT mice fed ethanol in the Lieber-DeCarli plan developed fatty liver, including liver triglyceride content increased, while mice lacking ecto-5'-nucleotidase or adenosine receptors A1 or A2B were protected against the development of fatty liver. Similar protection is also observed in WT mice treated with an antagonist of adenosine A1 and A2B. Steatotic livers showed increased expression of genes involved in fatty acid synthesis, which was prevented by blocking A1 adenosine receptors, and decreased the expression of genes involved in fatty acid metabolism, which was prevented by blocking adenosine A2B receptor.In vitro studies supported roles for adenosine A1 receptor in promoting the synthesis of fatty acids and A2B receptors by decreasing the metabolism of fatty acids. These results indicate that adenosine produced by ethanol metabolism plays an important role in ethanol-induced fatty liver via two receptors A1 and A2B, and suggest that targeting adenosine receptors can be effective in preventing the alcohol-induced liver fat.

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