Scientists may have uncovered part of the cause of some long-term lung diseases - and a possible target for future drugs.

Researchers say the CD44 molecule appears to play a key role in starting and stopping the inflammation of tissue which is important in the body's response to damage.

It is the persistence of this inflammation that contributes to chronic illness and longer-term damage to tissues.

One disease thought to work this way is chronic obstructive pulmonary disease (COPD), an incurable lung condition which affects mainly smokers.

The new role identified for CD44 is in an important clean-up process which follows the body's efforts to repair damaged tissue.

It is thought to help clear up waste cells from the injury, and call a halt to the inflammation, allowing scar tissue to be produced and the repair process completed.

In COPD, the inflammation persists, leading to damaging changes in lung tissues which cannot be reversed.

Altered mice

Researchers at the US Department of Veterans' Affairs have demonstrated the importance of the molecule for the first time in an animal study.

They "knocked out" the gene that produces CD44 in mice, then found that they developed inflammation that did not subside over time as it should.

Dr Paul Noble, one of the researchers, said: "This is helping us understand some of the basic healing mechanisms and what circumstances promote inflammation where more common causes like infection just aren't present."

'Exciting' news

Inflammation is a factor in many human illnesses, including asthma and rheumatoid arthritis, but it is not yet clear whether CD44 plays a similar role in these diseases, or even tissues outside the lung.

Dr Ian Dransfield, a reader in Medical Cell Biology at the University of Edinburgh, said that the finding was "exciting".

He said: "We have been interested in this for a number of years.

"What is different is that this team is concentrating on CD44's role clearing up waste cells rather than starting the inflammation process.

"If we could understand how CD44 is doing this, it may open new avenues for treatments."

The study was published in the journal Science.