ArticleAmerican journal of respiratory cell and molecular biology2008
A2B adenosine receptors regulate the mucus clearance component of the lung's innate defense system.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 52 citations in OpenAlex.
- Functional CFTR may be required for Prevotella melaninogenica regulation of epithelial cell defense against Staphylococcus aureus.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2026Article
- Purinergic receptors in airway hydration.Biochemical pharmacology · 2021Review
- CK2 is a key regulator of SLC4A2-mediated ClPflugers Archiv : European journal of physiology · 2017Article
- Purinergic Signaling in Mast Cell Degranulation and Asthma.Frontiers in pharmacology · 2017Review
- UDP-glucose promotes neutrophil recruitment in the lung.Purinergic signalling · 2016Article
- The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Uses its C-Terminus to Regulate the A2B Adenosine Receptor.Scientific reports · 2016Article
- Combination therapy with cystic fibrosis transmembrane conductance regulator modulators augment the airway functional microanatomy.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Physiological impact of abnormal lipoxin A₄ production on cystic fibrosis airway epithelium and therapeutic potential.BioMed research international · 2015Review
- Accumulation of metals in GOLD4 COPD lungs is associated with decreased CFTR levels.Respiratory research · 2014Article
- Bioinformatic Analysis of Differential Protein Expression in Calu-3 Cells Exposed to Carbon Nanotubes.Proteomes · 2013Article
- Nonantibiotic macrolides prevent human neutrophil elastase-induced mucus stasis and airway surface liquid volume depletion.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- A mechanochemical model for auto-regulation of lung airway surface layer volume.Journal of theoretical biology · 2013Article
- Roflumilast N-oxide, a PDE4 inhibitor, improves cilia motility and ciliated human bronchial epithelial cells compromised by cigarette smoke in vitro.British journal of pharmacology · 2012Article
- Rise of the sensors: nociception and pruritus.Current allergy and asthma reports · 2012Review
- Cigarette smoke exposure induces CFTR internalization and insolubility, leading to airway surface liquid dehydration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Suppression of adenosine-activated chloride transport by ethanol in airway epithelia.PloS one · 2012Article
- A pharmacologic approach to acquired cystic fibrosis transmembrane conductance regulator dysfunction in smoking related lung disease.PloS one · 2012Article
- Defective adenosine-stimulated cAMP production in cystic fibrosis airway epithelia: a novel role for CFTR in cell signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Prostaglandin E₂regulation of cystic fibrosis transmembrane conductance regulator activity and airway surface liquid volume requires gap junctional communication.American journal of respiratory cell and molecular biology · 2011Article
- Role of adenosine A(2B) receptors in inflammation.Advances in pharmacology (San Diego, Calif.) · 2011Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Adenosine (ADO) signaling is altered in both asthma and chronic obstructive pulmonary disease, and the A(2B) adenosine receptor (A(2B)-R) may drive pulmonary inflammation. Accordingly, it has been proposed that specific inhibition of the A(2B)-R could treat inflammatory lung diseases. However, stimulation of the cystic fibrosis transmembrane conductance regulator (CFTR) by ADO may be crucial in permitting the superficial epithelium to maintain airway surface liquid (ASL) volume, which is required to ensure hydrated and clearable mucus. Our goal was to determine which ADO receptor (ADO-R) underlies ASL volume regulation in bronchial epithelia. We used PCR techniques to determine ADO-R expression in bronchial epithelia and used nasal potential difference measurements, Ussing chambers studies, and XZ-confocal microscopy to look at Cl- secretion and ASL volume regulation. The A(2B)-R was the most highly expressed ADO-R in donor specimens of human bronchial epithelia, and inhibition of ADO-R in vivo prevented activation of CFTR. A(2B)-R was the only ADO-R detected in cultured human bronchial epithelial cells and inhibition of this receptor with specific A(2B)-R antagonists resulted in ASL height collapse and a failure to effect ASL height homeostasis. Removal of ADO with ADO deaminase and replacement with 5'N-ethylcarboxamide adenosine resulted in dose-dependent changes in ASL height, and suggested that the cell surface (ADO) may be in excess of 1 microM, which is sufficient to activate A(2B)-R. A(2B)-R are required for ASL volume homeostasis in human airways, and therapies directed at inhibiting A(2B)-R may lead to a cystic fibrosis-like phenotype with depleted ASL volume and mucus stasis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.