The reason why lungs of smokers are resistant to steroid treatment and its solution has been found by scientists from the Imperial College of London.

It is believed that almost 6 percent of population of the United Kingdom is presently suffering from Chronic Obstructive Pulmonary Disease (COPD) - ‘smoker’s lung’, or chronic bronchitis and emphysema. This is considered to be the fourth most cause of mortality in the land of the Queen.

Doctors generally consider steroid treatment as an effective treatment technique for curing inflammatory ailments such as COPD but somehow some of the COPD patients do not respond to steroid therapy as per expectations.

From News-Medical.Net:

Professor Peter Barnes and his colleagues discovered that steroids act as a ‘molecular bridge’ to recruit HDAC2 to the appropriate genes where it can act to switch them off.

The London researchers found that in COPD, levels of HDAC2 are very low compared to normal cells, so that the steroids have no effect in switching off the activated inflammatory genes.

They then found that in lung cells in vitro, and in rats, low doses of a cheap and widely available drug raised the levels of HDAC2 and broke the steroid resistance.

The first stages of clinical trials to test low doses of this drug, theophylline, in COPD patients are now underway. If successful, this may lead to a change in the treatment of COPD and other severe inflammatory diseases that do not respond well to steroid therapy.

Professor Peter Barnes commented, ‘COPD kills tens of thousands of people in the UK every year and currently we can only treat the symptoms, not the underlying problem of inflammation of the lungs. Our work has finally provided an explanation for steroid resistance in COPD, and has allowed us to identify ways to combat this.

Professor Peter Barnes and his colleagues remarked that steroids are highly effective in playing an important role while acting as molecular bridge in the recruitment of HDAC2 (Histone Deacetylase 2), an enzyme, to the concerned genes where it can switch them off.

They also remarked that the levels of HDAC2 are seen to be low when compared to normal cells in the COPD patients. This clearly suggested that the steroids are no longer good enough to bring any positive effect in switching off the activated inflammatory genes. In this direction, a new steroid has been discovered that will have the ability to raise the HDAC2 level to break steroid resistance in COPD patients.

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