Beta-agonists trigger T cell accumulation Source: J Allergy Clin Immunol 2006; (Monday, December 11, 2006)
Nov 28, 2006 - Bronchodilators appear to increase inflammation, potentially worsening asthma, heart failure, and lupus, study findings suggest.
In laboratory tests on peripheral blood lymphocytes (PBL), Raymond Penn (Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA) and colleagues showed that b-agonists, such as those used to treat asthma, increase the accumulation of type 2 T cells.
This is a pertinent finding, the scientists believe, as an over-reactive type 2 T cell response is thought to contribute to inflammatory diseases, such as asthma and lupus.
The researchers report in an advance online publication by the Journal of Allergy and Clinical Immunology, that when they added b-agonists to PBL cultured with interleukin (IL)-2, they saw an increased IL-2-induced accumulation of human type 2 T cells.
They suggest that, as b-agonists belong to a class of chemicals that includes adrenalin, the immune responses of patients with elevated adrenalin levels, such as those with emotional distress and heart failure, may also be altered, thus worsening disease.
“Inhaled b-agonists are very effective in opening up airways and allowing asthmatics to breathe, but their ability to address the underlying inflammation that causes most asthma has been debated for years,” said Penn.
In fact, many clinical trials have reported worsening symptoms in asthma patients on continuous b-agonist therapy. Current US Food and Drug Administration recommendations suggest asthma patients receiving long-acting b-agonists be supplemented with inhaled corticosteroids.
“From an asthma management standpoint, these studies further emphasize the need to include anti-inflammatory corticosteroids when treating moderate to severe asthma,” the researchers conclude.