Enzyme Offers New Treatment for Inflammatory Lung Disease
CHITIN, a compound known for its strength, can be destroyed by an enzyme secreted by the lungs according to results from a recent study. When chitinases, enzymes that are responsible for breaking down chitin and disposing of it, are not present in mice, they soon experience a build-up of chitin in their lungs, which can cause them to develop severe inflammatory lung disease. Researchers did however find that by restoring the missing chitinases, either genetically or with drugs, lung function could be improved.
Dr Richard Locksley, University of California San Francisco, San Francisco, California, USA, commented: “We were very excited to see that improving chitinase activity quickly cleared up the signs of chronic inflammatory lung disease in these mice.” He continued: “To our knowledge this is the first demonstration that chitinases play a key role in preserving lung function in vertebrates.” Previous studies conducted by Locksley’s lab have highlighted that lung inflammation in mice can be triggered by chitin.
In this study, chitin was found to build up in mice that were genetically modified to lack AMCase, a chitinase enzyme produced in the airways of mice. This resulted in a chronic inflammatory immune response as well as the triggering of cellular stress pathways that have been previously associated with human lung disease. When mice lacked AMCase, they died at a significantly younger age than control mice. Furthermore, adult mice were demonstrated not to tolerate chitin-triggered inflammation as well as younger mice, as they displayed a rapid decline in health and signs of advancing fibrotic lung disease.
Inflammatory lung disease in humans was also studied and an increased level of chitin was found in the lungs of patients with inflammatory lung disease. Although researchers did not find reduced chitinase activity levels to be any lower in patients with inflammatory lung disease, they have hypothesised that the lung’s ability to use chitinases to remove chitin is reduced by age-associated lung fibrosis. Results have been viewed with excitement about the potential for future therapy that this study has offered. They hope that enhancing chitinases activity with drugs will lead to a new treatment modality for fibrotic lung disease; this is something that is especially pertinent as currently there are no highly efficacious treatments.