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10.1073/pnas.1710196114

http://scihub22266oqcxt.onion/10.1073/pnas.1710196114
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C5664525!5664525!29073113
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suck abstract from ncbi


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pmid29073113      Proc+Natl+Acad+Sci+U+S+A 2017 ; 114 (43): E9163-71
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  • ?2-Adrenoceptor signaling in airway epithelial cells promotes eosinophilic inflammation, mucous metaplasia, and airway contractility #MMPMID29073113
  • Nguyen LP; Al-Sawalha NA; Parra S; Pokkunuri I; Omoluabi O; Okulate AA; Windham Li E; Hazen M; Gonzalez-Granado JM; Daly CJ; McGrath JC; Tuvim MJ; Knoll BJ; Dickey BF; Bond RA
  • Proc Natl Acad Sci U S A 2017[Oct]; 114 (43): E9163-71 PMID29073113show ga
  • Activation of ?2-adrenoreceptors (?2ARs) on airway smooth muscle cells produces airway relaxation, and ?2AR agonists are the most widely used bronchodilators for treating asthma. Paradoxically, murine models show ?2AR activation is also required for expression of cardinal features of the asthma phenotype, including airway hyperresponsiveness (AHR), inflammation, and mucous metaplasia. However ?2ARs are expressed on all the cell types implicated in the pathogenesis and maintenance of asthma, and which cell type(s) control these asthmatic effects is unknown. Here we show activation of ?2AR signaling solely on airway epithelium is sufficient to restore/promote the cardinal features of asthma, including inflammation, mucous metaplasia, and AHR. These studies support the role of the airway epithelium as a master regulator of key features of asthma.
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