Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3198560 | Journal of Allergy and Clinical Immunology | 2012 | 22 Pages |
Abstract
Nicotine-induced airway mucus formation is independent of IL-13, and α7-nAChRs are critical in airway mucous cell metaplasia/hyperplasia and mucus production in response to various promucoid agents, including IL-13. In the absence of nicotine, acetylcholine might be the biological ligand for α7-nAChRs to trigger airway mucus formation. α7-nAChRs are downstream of IL-13 but upstream of GABAARα2 in the MUC5AC pathway. Acetylcholine and α7-nAChRs might serve as therapeutic targets to control airway mucus.
Keywords
Tris-buffered saline containing 0.05% Tween-20AB/PASqPCRNHBETBSTGAPDHTCrPICMLAnAChROVAQuantitative PCRSmall interfering RNAsiRNAAcetylcholineAliOvalbuminnormal human bronchial epithelialImmunohistochemistryIHCSecondhand smokeCigarette smokemethyllycaconitineAirway mucusMecamylamineNicotineair-liquid InterfacePicrotoxinGABAARglyceraldehyde-3-phosphate dehydrogenasenicotinic acetylcholine receptorT-cell receptornicotinic acetylcholine receptorsγ-Aminobutyric acid receptors
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Authors
Sravanthi MS, Julie A. PhD, Neerad C. PhD, Jules MS, Raymond J. PhD, Shashi P. PhD, Ali Imran MD, Richard J. BS, Katherine M. BS, Juan Carlos BS, Kevin S. PhD, J. Michael PhD, Shilpa PhD, Mohan L. PhD,