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A New Player In The Battle Against Hepatitis Prevents Inflammation And The Death Of Liver Cells

Date:
September 5, 2005
Source:
VIB, Flanders Interuniversity Institute of Biotechnology
Summary:
Scientists from the Flanders Interuniversity Institute for Biotechnology (VIB) have again achieved a breakthrough in research on hepatitis. The researchers, connected to Ghent University, have discovered the function of one of the most important proteins involved in hepatitis. Using a mouse model, they have shown that the protein prevents inflammation of the liver as well as the death of liver cells. This discovery can form the basis for the development of a new therapy in the battle against hepatitis in humans.

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Hepatitis, a liver disorder

Hepatitisis a collective term for a number of inflammations of the liver whosesymptoms strongly resemble each other. These inflammations can have awide variety of causes, such as alcohol abuse or infection by ahepatitis virus. Hepatitis B and C, for example, are caused by a virusthrough contact with the blood or other bodily fluids of infectedpersons. In some cases, the person remains a carrier of the virus, andchronic hepatitis and even cancer of the liver can develop.

InBelgium, at least 700,000 people have had hepatitis B, and 5%-10% ofthese persons are still chronic carriers of the virus. Each year, thereare about 6000 new infections. The number of people with hepatitis Ccomes to 80,000-100,000 - and 60%-80% of these persons develop chronichepatitis. There is a vaccination against hepatitis B, but none againsthepatitis C.

A new role for the protein ABIN-1

TNF(Tumor Necrosis Factor) is produced by our body, normally in smallquantities. In inflammations of the liver, excessive TNF productionactivates the mechanisms that lead to inflammation and the death ofliver cells and liver tissue. In addition, excessive TNF in liver cellsstimulates the protein NF-ƒkB, which is also responsible for theinflammation of the liver. This makes NF-ƒkB an attractive target for atherapy that would neutralize the inflammation. However, an idealtherapy also needs to prevent the death of the liver cells.

Thenew player that this research brings a step closer to the realizationof such a therapy is the protein ABIN-1. From previous research by theVIB research group - led by Rudi Beyaert - it turns out that ABIN-1inhibits the action of NF-ƒkB. Now, Andy Wullaert and severalcolleagues from this team have shown that an extra dose of ABIN-1provides a double protection to liver cells in mice. With an elevatedproduction of ABIN-1, this protein will neutralize the inflammationcaused by NF-ƒkB and also prevent the complete death of liver cellsafter induction by TNF.

ABIN-1 in the treatment of liver disorders

Thisresearch discloses the double protective action of ABIN-1 in liverdisorders. NF-ƒkB, also responsible for inflammations, is inhibited byan elevated presence of ABIN-1. In addition, ABIN-1 also counteractsthe death of liver cells. Further research can lead to new therapies inthe battle against hepatitis, through which - by increasing thepresence of ABIN-1 in the liver - one can inhibit the inflammation andprevent dell death.


Story Source:

The above story is based on materials provided by VIB, Flanders Interuniversity Institute of Biotechnology. Note: Materials may be edited for content and length.


Cite This Page:

VIB, Flanders Interuniversity Institute of Biotechnology. "A New Player In The Battle Against Hepatitis Prevents Inflammation And The Death Of Liver Cells." ScienceDaily. ScienceDaily, 5 September 2005. <www.sciencedaily.com/releases/2005/09/050904230438.htm>.
VIB, Flanders Interuniversity Institute of Biotechnology. (2005, September 5). A New Player In The Battle Against Hepatitis Prevents Inflammation And The Death Of Liver Cells. ScienceDaily. Retrieved December 19, 2014 from www.sciencedaily.com/releases/2005/09/050904230438.htm
VIB, Flanders Interuniversity Institute of Biotechnology. "A New Player In The Battle Against Hepatitis Prevents Inflammation And The Death Of Liver Cells." ScienceDaily. www.sciencedaily.com/releases/2005/09/050904230438.htm (accessed December 19, 2014).

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