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- W2177742114 abstract "Asthma is one of the most common of medical illnesses and is treated in part by drugs that activate the beta-2-adrenoceptor (β2-AR) to dilate obstructed airways. Such drugs include long acting beta agonists (LABAs) that are paradoxically linked to excess asthma-related mortality. Here we show that LABAs such as salmeterol and structurally related β2-AR drugs such as formoterol and carvedilol, but not short-acting agonists (SABAs) such as albuterol, promote exaggerated asthma-like allergic airway disease and enhanced airway constriction in mice. We demonstrate that salmeterol aberrantly promotes activation of the allergic disease-related transcription factor signal transducer and activator of transcription 6 (STAT6) in multiple mouse and human cells. A novel inhibitor of STAT6, PM-242H, inhibited initiation of allergic disease induced by airway fungal challenge, reversed established allergic airway disease in mice, and blocked salmeterol-dependent enhanced allergic airway disease. Thus, structurally related β2-AR ligands aberrantly activate STAT6 and promote allergic airway disease. This untoward pharmacological property likely explains adverse outcomes observed with LABAs, which may be overcome by agents that antagonize STAT6." @default.
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- W2177742114 date "2015-11-25" @default.
- W2177742114 modified "2023-10-15" @default.
- W2177742114 title "Long-Acting Beta Agonists Enhance Allergic Airway Disease" @default.
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- W2177742114 doi "https://doi.org/10.1371/journal.pone.0142212" @default.
- W2177742114 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4659681" @default.
- W2177742114 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26605551" @default.
- W2177742114 hasPublicationYear "2015" @default.
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