Inhaled beta2-agonists and airway responses to allergen

A series of investigations show that the regular use of inhaled beta2-agonists will increase all aspects of the airway response to allergen. The mechanism of this effect is uncertain; however, it appears to be different from the mechanism that produces tolerance to beta2-agonist effects. One possibility is that the regular use of beta2-agonists might induce a mast cell beta-receptor dysfunction that might make mast cells more prone to release mediators. As a result beta2-agonist use plus allergen exposure might cause more mediator release than does allergen exposure alone. The corollary of this is that beta2-agonist use plus allergen exposure might cause more airway inflammation than does allergen exposure alone. These hypotheses are both testable. I believe that this is a clinically important phenomenon and may well be a major reason for beta2-agonist-induced worsened asthma control. Further investigations are indicated to identify the mechanism and the clinical relevance of the phenomenon.