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Discovery of key inflammation mechanism in COPD could lead to new treatments


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Under embargo for
22.00 BST/17.00EST
Wednesday 11 May 2005

An international team of researchers has identified a mechanism which increases lung inflammation, making Chronic Obstructive Pulmonary Disorder (COPD) more severe, and potentially points towards new treatments.

Reporting today in the New England Journal of Medicine, the team from Imperial College London, Royal Brompton Hospital and the University of British Columbia, Canada found a correlation between the increase in inflammation in the lungs and a loss of activity in an enzyme responsible for switching off inflammatory genes and cells, called histone deacetylase (HDAC).

Professor Peter Barnes, from Imperial College London and the Royal Brompton Hospital, and senior author of the research, said: "COPD is the only common cause of death in the western world that is increasing, affecting almost a million patients in the UK, and four million in the USA, and the identification of this molecular mechanism could be of enormous importance in how we treat COPD in the future."

The team believe that the loss of HDAC activity may also explain why COPD is not responsive to steroids, as steroids require HDAC in order to switch off the inflammation.

Previous research by Professor Barnes has shown that low doses of theophylline, a substance occurring in tea leaves which helps relax the bronchial tubes, could help restore HDAC activity, and potentially reverse the resistance to steroids.

Professor Barnes adds: "Although this research is at a fundamental level, the discovery that COPD affects HDAC activity, which in turn can be affected by theophylline, could be the first step towards the development of an effective treatment."

The researchers looked at lung tissue samples from 40 patients with a range of different COPD stages.

The research was supported by grants from the British Lung Foundation, Asthma UK, GlaxoSmithKline, Boehinger Ingelheim, Mitsubishi Pharma and the Canadian Institutes of Health Research.

For further information please contact:

Tony Stephenson
Press Officer
Communications Department
Tel: +44 (0)20 7594 6712
Mobile: +44 (0)7753 739766
E-mail: at.stephenson@imperial.ac.uk

Notes to editors:

Decreased Histone Deacetylase Activity and Chronic Obstructive Pulmonary Disease, New England Journal of Medicine, 11 May 2005.

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