In vivo, epithelial cells express fewer adhesion molecules after second-generation antihistamine treatment. In a murine model of asthma, antihistamines inhibited the Th2 response, lung inflammation, and AHR. Antihistamines further afforded broncho-protection against methacholine challenge. Antihistamines could possibly be useful in preventing the development of asthma in certain patients as reported in cohorts of children with atopic dermatitis. Other antiallergic molecules such as cromolyn and nedocromil stabilize mast-cell membrane and therefore decrease mediator release. Although it might be of interest to determine whether they could play a role in the prevention of remodeling, up to now we have no data indicating that they may affect bronchial structural changes (Table 3). in detail
P2-Agonists reduce airway muscular tone and improve expiratory flow. Combinations of long-acting P2-agonists (LABAs) and low-dose ICS result in a similar control of the disease and reduction of in-duced-sputum inflammatory features compared with moderate doses of ICS after 1 year of treatment. LABAs alone modestly decrease airway eosinophilia. The number of airway total leukocytes and mast cells increases after allergen challenge in patients receiving a LABA only. (32-Agonists induce a change in response toward a Th2 profile in human peripheral blood mononuclear cells by increasing Th2 cytokine expression. Overall, (32-agonists are not considered to have significant antiinflammatory properties. In regard to remodeling, however, until recently we had little evidence that they may affect airway structure. However, one study suggested that salmeterol could lead to a reduction in airway vasculature. As for theophylline, although an immunomodulatory effect has been suggested, we have no evidence regarding its influence on airway remodeling, although long-term studies have yet to be conducted.