Harmful Cells May Have A Role To Play In Liver Repair, Study Suggests

Main Category: Liver Disease / Hepatitis
Also Included In: Biology / Biochemistry
Article Date: 18 Jan 2013 - 0:00 PST


Liver damage could be repaired by the same cells that harm the organ in the first place, a study suggests.

The cells - called macrophages - cause tissue to become scarred, which can lead to cirrhosis of the liver.

Scientists at the University of Edinburgh have now found that the macrophages also have a role in breaking down and getting rid of damaged tissue so that the normal liver structure and function is restored.

Macrophages are found throughout the body and help fight infection by breaking down bacteria. They also regulate inflammation in cells, which can cause scarring in tissue and help to seal wounds.

Researchers are identifying what triggers the cells to change their function in the liver, with a view to developing a drug that switches the cells to repair mode.

Liver cirrhosis occurs as a result of long-term damage that can be brought on by infection, excess alcohol consumption or obesity. The condition, which is increasing rapidly, currently ranks as the 5th most common cause of death leading to around 1,000 deaths in the UK each year, with 700 people needing a transplant to survive.

Prakash Ramachandran, of the University of Edinburgh's MRC Centre for Inflammation Research, said: "We have shown that the very cells that provoke scarring to the liver can also help the liver to heal by getting rid of damaged tissue.

"While scarring of the skin, for instance, following a cut is important to help the skin heal when the liver becomes scarred this can affect how it works, preventing toxins in the bodies from being broken down properly."

The study, which has been published in PNAS, looked at the role of macrophages in liver tissue in mice.

The research was funded by the Medical Research Council, the Wellcome Trust, the Academy of Medical Sciences, the Health Foundation, Royal College of Surgeons of Edinburgh, British Heart Foundation and Sir Jules Thorn Trust.

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