Could a common class of drugs used for acute asthma attacks be causing the very thing it aims to treat?
Perhaps, find researchers from Harvard School of Public Health and Brigham and Women's Hospital who studied the use of bronchodilators known as beta-agonists in asthmatics.
Beta-agonists are the primary treatment used to relieve acute asthma attacks. The drugs come in many forms -- they may be delivered with an inhaler, given in pill or liquid form, delivered in a nebulizer, or given by injection. Whatever the mode of administration, they work by relaxing the airway and reducing airway responsiveness to allergens that cause it to restrict and cause an acute attack. Many people with asthma rely heavily on these medications, sometimes taking them several times a day. Previous research suggests regular use could increase sensitivity to airway constriction and thus lead to a greater number of attacks and more serious attacks, primarily by causing a desensitization of the beta2-adrenergic receptor (beta2AR) that the drug binds with to achieve its effects.
These researchers suggest an alternative mechanism. Their study finds the increased airway hyperresponsiveness seen in some regular users of beta-2 agonists may be due to increased expression of a substance called phospholipase C-beta (PLC-beta) in the smooth airway muscle that occurs with persistent high-level activation of the beta2AR. The finding may lead to new treatments for asthma targeting PLC-beta.
Writing in an accompanying commentary, other researchers from Harvard and Brigham and Women's concur, noting, "Understanding the panoply of beta2AR-mediated events in airway smooth muscle might lead to the design of new agonists that avoid negative effects of beta2AR activation while enhancing events that lead to relaxation."