Root cause of inflammatory diseases discovered

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Press Trust of India London
Last Updated : Jan 24 2013 | 2:11 AM IST

Researchers from the University of East Anglia (UEA) who made this discovery said their work could eventually lead to new treatments for chronic inflammatory diseases.

Cardiovascular disease arising from atherosclerosis, or thickening of the arteries, kills around 17 million people worldwide each year, while rheumatoid arthritis affects around 400,000 people in the UK alone.

The UEA team studied a type of white blood cell, called monocytes, that play a key role in the human immune system and help protect our bodies against infection. But they can also invade tissue, triggering the early stages of common inflammatory diseases.

The team detected for the first time that monocytes were surrounded by a constant cloud, made up of potent inflammatory molecules called adenosine triphosphate, or ATP.

Further study showed that the ATP molecules were being propelled through the cell wall by the actions of lysosomes -- sub-cellular compartments within blood cells which had earlier been thought to only break down cell waste.

"These unexpected findings shed light on the very early stages in the development of inflammatory diseases such as atherosclerosis and rheumatoid arthritis," said lead author Dr Samuel Fountain of UEA's School of Biological Sciences.

"We found that lysosomes are actually highly dynamic and play a key role in the way inflammatory cells function. This is an exciting development that we hope will lead to the discovery of new targets for inflammatory drugs in around five years and potential new treatments beyond that."

However, Dr Fountain said further study was now needed to investigate how to control the release of ATP by lysosomes in monocytes and other white blood cells, and it's also important to understand how inflammation may be affected in patients with inherited diseases involving lysosomes.

The new findings are published in The Journal of Cell Science.

  

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First Published: Jul 05 2012 | 4:36 PM IST

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