An international team of researchers has identified a biological mechanism that increases lung inflammation, making chronic obstructive pulmonary disorder (COPD) more severe, say researchers, who hope this finding will lead toward 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).

"COPD is the only common cause of death in the western world that is increasing, affecting almost 1 million patients in the U.K., and 4 million in the U.S., and the identification of this molecular mechanism could be of enormous importance in how we treat COPD in the future," says senior author of the research, Peter Barnes, professor at Imperial College London and Royal Brompton Hospital.

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

Previous research by 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.

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 toward 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.

Source: Imperial College London