Tests on mice have given German researchers fresh hope that existing drugs could be used to reverse the debilitating effects of emphysema but experts have cautioned that the results may not apply to humans.
Sufferers of chronic obstructive pulmonary disease (COPD), which includes chronic bronchitis and emphysema, often have difficulty breathing without an oxygen tank. Millions die every year from the disease, which is commonly caused by smoking.
In a study published today by the journal Cell, scientists showed that an enzyme called nitric oxide synthase (iNOS) can cause high blood pressure and changes to pulmonary blood vessels that lead to emphysema.
Mice that did not have the enzyme in their bodies did not develop emphysema, they said.
Existing drugs that block the iNOS enzyme also reversed the condition in mice that were already sick, the study found.
“Our data indicate that targeting iNOS by pharmacological inhibition can improve the functional and structural destruction caused by tobacco smoke,” the study said.
The researchers plan new experiments to develop a drug that can be inhaled for treatment of emphysema in humans, but Professor Gary Anderson from the University of Melbourne’s Lung Disease Research Group urged caution.
“It’s a very well designed study executed to a high technical standard but we need to have some serious reservations about translation to humans,” he said.
“The lung regeneration is interesting but mice have a very large capacity for regeneration which is absent in humans.”
Professor Paul Thomas from the University of NSW’s Infection and Inflammation Research Centre said the study suggested a potential new avenue of treatment for emphysema.
“The use of iNOS inhibitors is quite feasible – we and others have shown that is possible to inhibit iNOS by inhaling such drugs. One problem in applying this possible therapy to humans may be that most patients with COPD are often treated with steroids (prednisolone, budesonide, fluticasone) either orally or by inhaled therapy, and these drugs are potent inhibitors of iNOS also. There are no data to suggest that this steroid-induced inhibition has marked effects in man in this disease,” he said.
“Thus, the effect of an iNOS inhibitor may be modest, but it is worth exploring in this disease which is difficult to treat. Smoking cessation remains the cornerstone to stopping the development of COPD.”