Asthma, Author Interviews / 26.07.2016
Loss of ADAM33 suppresses features of asthma, suggesting targeting ADAM33 as a potential new asthma therapy
MedicalResearch.com Interview with:
Hans Michael Haitchi, MD, MMed (INT)
PhD, PD, FHEA, PGcert
Associate Professor in Respiratory Medicine
Clinical and Experimental Sciences
Faculty of Medicine, University of Southampton
United Kingdom
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: It is estimated that 300 million people worldwide suffer from asthma with 1 in 10/11 (USA/UK) children and 1 in 12 (USA & UK) adults suffering from the disorder. In children asthma is the most common long-term medical condition.
ADAM33 is an asthma gene. Small changes in the gene have been associated with increased twitchiness of the airways (bronchial hyperresponsiveness), loss of lung function in children and decline in lung function in the general population.
ADAM33 makes an enzyme, which is attached to cells in the airway muscles. When the enzyme loses its anchor to the cell surface, it is prone to going rogue around the lung causing poorer lung function in people who have asthma.
Our research, published in The Journal of Clinical Investigation (JCI) Insight, analysed human tissue samples and mice. Our experiments suggest that the human rogue ADAM33 protein is increased and enzymatically active in asthma. Furthermore, ADAM33 protein initiates airway remodelling (more muscle and blood vessels around the airways) without causing any inflammation in early life. However, when we switch off ADAM33 or prevent it from going rouge, the features of asthma - airway remodelling (more muscle and blood vessels around the airways), twitchiness and inflammation - will be reversed or reduced.
These findings identify ADAM33 as a novel target for disease modifying therapy in asthma.
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