A process to repair lungs damaged by asthma is being developed by researchers in the United Kingdom.
Dr Tara Sutherland, from the University of Aberdeen, said a study into the scarring that occurred in lung tissue as a result of asthma had resulted in a process able to reverse these changes in animal models.
Dr Sutherland said current treatments for asthma largely involved controlling the inflammation of lung tissue using steroid inhalers, but this breakthrough offered a potential new way to treat asthma symptoms and even repair previously irreversible lung damage.
“Although still in the early stages of development, this discovery paves the way for a new way to treat not only asthma, but many different diseases in which similar structural changes in tissues occur, such as chronic obstructive pulmonary disease (COPD), chronic heart disease and cirrhosis of the liver.”
She said even when treated, asthma could be fatal, despite the availability of new treatments which aimed to dampen down inflammation in the lungs.
“However, as well as inflammation, asthma also results in what has previously been considered to be irreversible structural lung changes.”
Dr Sutherland said these changes included making the lungs stiffer and more scarred through increases in things like “extracellular matrix collagens”.
She said using animal models that shared features of severe asthma in people, the researchers found that preventing inflammation alone was not enough to reverse this tissue scarring and discovered blocking the action of specific protein molecules strongly associated with inflammation and tissue damage, “remarkably reversed” scarring in the lungs.
“Drugs that inhibit inflammation in asthma are crucial for managing the disease. However, these drugs may not always be enough to prevent and reverse lung damage found in severe asthma.
“Our findings show that we also need to consider that structural lung changes occur in severe asthma and that these changes may occur independently of inflammatory pathways.”
Read the full study: Allergen-induced airway matrix remodeling in mice can be prevented or reversed by targeting chitinase-like proteins.
