New research from the University of Southampton is intended to expand the researchers’ knowledge about why some individuals are more prone to develop asthma by analyzing a specific gene. The gene, called ADAM33, is often linked to the development of the condition and its characteristic airway “twitchiness,” and is also believed to impact the airway architecture in young children’s lungs. The study will assess mice that were born with and without the ADAM33 enzyme, exposing the mice to causes of allergic inflammation, like dust allergens or the interleukin-13 protein, as indicated on a Lung Disease News report.

This strategy will enable researchers to learn how the enzyme causes airway remodeling and is involved in lung inflammation caused by allergens early in life. The research team will use genetic methods to analyze the lungs of the animals, with the expectation that it may lead to the discovery of new asthma disease-linked genes and respective proteins. Lead researcher Michel Haitchi says, “We know that ADAM33 makes an enzyme, which is attached to cells in the airway muscles. In asthma, it has been found that this enzyme goes rogue from these cells and higher levels of the enzyme are associated with poorer lung function.”

Furthermore, Haitchi says, “We think that when it detaches it causes problems by affecting cells that shouldn’t come into contact with it and this results in subtle changes in the airway wall – called airway remodeling – involving over-growth of cells that cause the airways to narrow, among other asthma-associated changes. We also think that this airway remodeling can occur before birth, which is something we will focus on in the study.” Haitchi explains the team wanted to see how the remodeling affects reactions to irritants later in life.

“Understanding how the ADAM33 enzyme causes airway remodeling before birth and the responses to environmental triggers such as allergens are the first steps in developing a treatment to stop this from happening,” Haitchi says. “Airway remodeling reduces the ability of the lungs to function, and is not prevented by current anti-inflammatory steroid therapy. Therefore, stopping this would prevent a harmful effect of asthma for many of the 5.4 million people in the UK with the condition.”

Samples from young children whose mothers have asthma as well as children who have the condition will be also be included in the study to evaluate how the ADAM33 enzyme interacts with the airway structure. Samantha Walker, PhD, director of research and policy at Asthma UK, states, “This project has the potential to make a real difference to people’s lives in the future by preventing them from developing asthma in the first place.”

Source: Lung Disease News