Albuterol Amplifies Airway Hyperresponsiveness in an Allergic Asthma Model.

Lundblad, LK; Rinaldi, Lisa; Norton, RJ; Riesenfeld, Erik; Poynter, M.E.; Barone, LM; Cg, Irvin

doi:10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2414

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“…To test the hypothesis that albuterol increases airways hyperresponsiveness in inflamed lungs, we studied the effect of long-term inhaled albuterol stereoisomers on respiratory reactivity in mouse models of asthma, including immediate allergic response (IAR) and allergen induced airways hyperresponsiveness (AHR). Some of the data were previously presented in preliminary form as abstracts at the 2008 and 2009 American Thoracic Society meetings [ 13 , 14 ] and the 2008 IDEA meeting [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Detrimental effects of albuterol on airway responsiveness requires airway inflammation and is independent of β-receptor affinity in murine models of asthma

et al. 2011

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BackgroundInhaled short acting β2-agonists (SABA), e.g. albuterol, are used for quick reversal of bronchoconstriction in asthmatics. While SABA are not recommended for maintenance therapy, it is not uncommon to find patients who frequently use SABA over a long period of time and there is a suspicion that long term exposure to SABA could be detrimental to lung function. To test this hypothesis we studied the effect of long-term inhaled albuterol stereoisomers on immediate allergic response (IAR) and airway hyperresponsiveness (AHR) in mouse models of asthma.MethodsBalb/C mice were sensitized and challenged with ovalbumin (OVA) and then we studied the IAR to inhaled allergen and the AHR to inhaled methacholine. The mice were pretreated with nebulizations of either racemic (RS)-albuterol or the single isomers (S)- and (R)-albuterol twice daily over 7 days prior to harvest.ResultsWe found that all forms of albuterol produced a significant increase of IAR measured as respiratory elastance. Similarly, we found that AHR was elevated by albuterol. At the same time a mouse strain that is intrinsically hyperresponsive (A/J mouse) was not affected by the albuterol isomers nor was AHR induced by epithelial disruption with Poly-L-lysine affected by albuterol.ConclusionsWe conclude that long term inhalation treatment with either isomer of albuterol is capable of precipitating IAR and AHR in allergically inflamed airways but not in intrinsically hyperresponsive mice or immunologically naïve mice. Because (S)-albuterol, which lacks affinity for the β2-receptor, did not differ from (R)-albuterol, we speculate that isomer-independent properties of the albuterol molecule, other than β2-agonism, are responsible for the effect on AHR.

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Section: Introductionmentioning

confidence: 99%