Share on FacebookTweet about this on TwitterShare on Google+Share on RedditShare on LinkedInShare on Tumblr

Asthma is a chronic condition that affects the airways in our lungs. In people with asthma, these airways constrict due to irritation caused by inflammation and airway remodeling–structural changes that cause the thickening of airway walls and subsequent narrowing of the airways. According to the CDC, 1 in every 13 people in the United States has asthma. The prevalence of asthma has been steadily increasing since 2001, and is currently at it’s highest recorded level, with no definitive explanation for the rise. Research towards a cure for the disease could greatly improve the lives of the more than 25 million people with asthma in the U.S. alone.

Scientists at the University of Southampton have discovered a way to stop asthma, or at least significantly reduce its effects, at the source: the ADAM33 gene. ADAM33 has been associated with asthma and bronchial hyper-responsiveness, with higher levels of expression related to greater severity of asthma and reduced lung function. The gene results in the production of the enzyme sADAM33, which has been found in high levels in smooth muscle and fibroblasts in lung airways, suggesting that the gene may play a direct role in airway remodeling.

 Healthy human lungs

Image Source: Science Photo Library – ANDRZEJ WOJCICKI

The researchers confirmed this when they induced the expression of sADAM33 in mice and observed resultant airway remodeling. The scientists also found that airway remodeling resulting from sADAM33 expression being switched on in utero was completely reversible if the gene was later switched off. Performing the same studies in human lung tissue cultures, the researchers observed the same changes in airway remodeling. In another study where ADAM33 was removed in mice, the researchers observed a significant reduction in inflammation and airway remodeling after exposure to an allergen. The researchers concluded that while airway remodeling did not directly cause inflammation, the resulting changes led to increased sensitivity to allergens and greater numbers of fibroblasts and smooth muscle cells (which contribute to inflammation), which suggests that airway remodeling promotes inflammation; this is in contrast to the previously held belief that inflammation causes remodeling.

While current asthma treatments focus mainly on inflammation, the results of this study make a strong case for targeting ADAM33 to prevent airway remodeling. Developing a therapy that successfully suppresses the expression of this gene could be a highly effective treatment for asthma.

Feature Image Source: Inhaler by Ben Dalton

Share on FacebookTweet about this on TwitterShare on Google+Share on RedditShare on LinkedInShare on Tumblr