Discovery of inflammation mechanism could lead to new treatments for COPD
12 May 2005
An international team, including researchers from Imperial College, has identified a mechanism that increases lung inflammation, making Chronic Obstructive Pulmonary Disorder (COPD) more severe and pointing to potential new treatments.
Reporting in the 11th May issue of the New England Journal of Medicine, the team from Imperial College, the Royal Brompton Hospital and the University of British Columbia, Canada, found a correlation between increased 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 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 believes 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 occuring 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, Boehringer Ingelheim, Mitsubishi Pharma and the Canadian Institutes of Health Research.
