By Mohamad Hamze
Researchers at the Houston Methodist Research Institute have elucidated a new potential drug target for asthma sufferers that could radically change the way patients manage their condition. Asthma’s characteristic effects include an excess of airway-lubricating and protecting mucin that makes breathing difficult, but the mechanism of this overproduction has only just recently been published Xian C. Li, M.D., Ph.D and team of Houston Methodist’s Immunobiology and Transplant Science Center.
In the February 5th edition of the Journal of Experimental Medicine, Dr. Li published his team’s findings on the effects of the helper T cell on mucin-producing cells in the airway, which communicate via the small molecule interleukin 9 (IL-9) in T cells. The article explains how asthma patients’ hyperactive T cells express the OX40 stimulatory ligand, which induce super-enhancers of the gene that encodes for IL-9. Thus, mucin production is upregulated in the epithelial lining of the airway, causing airway inflammation and constriction.
What this knowledge carries, Li suggests, is the possibility of targeting and blocking the effects of these IL-9 super-enhancers somewhere in that pathway to reduce inflammation and relieve both chronic and acute asthma symptoms. Even with a wide range of steroid and bronchodilator treatments currently available, many of the estimated 300 million asthma sufferers worldwide still find it difficult to control their conditions, so Li hopes that development of targeted drug therapies with this new model has the potential to be more direct and “more efficacious than the [current] standard of care.”
Houston Methodist. "New explanation for why airways close in asthma holds promise for future class of drugs." ScienceDaily. ScienceDaily, 31 January 2018.