Friday 03, Jul 2009
Why Lungs of Smokers are resistant to Steroid Treatment?
Posted Byi steroids
Scientists from the Imperial College, London have found the reason why lungs of smokers are resistant to steroid treatment along with finding a solution to this resistance.
Chronic Obstructive Pulmonary Disease (COPD) - ‘smoker’s lung’, or chronic bronchitis and emphysema - presently affects 6 percent population of the United Kingdom and is considered to be the fourth most common death cause in the land of the Queen.
It is seen that steroids are normally very effective in the treatment of inflammatory ailments such as COPD but some COPD patients do not respond as per expectations to steroid therapy.
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 found out that steroid are effective in playing an active role for acting as a molecular bridge in the recruitment of Histone Deacetylase 2 (HDAC2), an enzyme, to the relevant genes where it can switch them off.
They also discovered that levels of HDAC2 were very low compared to normal cells in the COPD patients. This means that the steroids are no longer potent enough to have any effect in switching off the activated inflammatory genes. In this direction, a new steroid has been found that can raise the levels of HDAC2 and break the resistance of steroids.
Tags: chronic bronchitis, chronic obstructive pulmonary disease, COPD, emphysema, smoker’s lung, steroid therapy, steroid treatment, steroids
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