NDLI: Alveolar Epithelial A2B Adenosine Receptors in Pulmonary Protection during Acute Lung Injury.

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Alveolar Epithelial A2B Adenosine Receptors in Pulmonary Protection during Acute Lung Injury.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Brodsky, Kelley S. Zwissler, Bernhard Eltzschig, Holger K. Hoegl, Sandra Blackburn, Michael R. Karmouty-Quintana, Harry
Description	Author Affiliation: Hoegl S ( Organ Protection Program, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, CO 80045); Brodsky KS ( Organ Protection Program, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, CO 80045); Blackburn MR ( Health Science Center at Houston, University of Texas, Houston, TX 77030.); Karmouty-Quintana H ( Health Science Center at Houston, University of Texas, Houston, TX 77030.); Zwissler B ( Department of Anesthesiology, Comprehensive Pneumology Center Munich, German Center for Lung Research, University Hospital, Ludwig Maximilian University, D-81377 Munich, Germany); Eltzschig HK ( Organ Protection Program, Department of Anesthesiology, University of Colorado School of Medicine, Aurora, CO 80045)
Abstract	Acute lung injury (ALI) is an acute inflammatory lung disease that causes morbidity and mortality in critically ill patients. However, there are many instances where ALI resolves spontaneously through endogenous pathways that help to control excessive lung inflammation. Previous studies have implicated the extracellular signaling molecule adenosine and signaling events through the A2B adenosine receptor in lung protection. In this context, we hypothesized that tissue-specific expression of the A2B adenosine receptor is responsible for the previously described attenuation of ALI. To address this hypothesis, we exposed mice with tissue-specific deletion of Adora2b to ALI, utilizing a two-hit model where intratracheal LPS treatment is followed by injurious mechanical ventilation. Interestingly, a head-to-head comparison of mice with deletion of Adora2b in the myeloid lineage (Adora2b(loxP/loxP) LysM Cre(+)), endothelial cells (Adora2b(loxP/loxP) VE-cadherin Cre(+)), or alveolar epithelial cells (Adora2b(loxP/loxP) SPC Cre(+)) revealed a selective increase in disease susceptibility in Adora2b(loxP/loxP) SPC Cre(+) mice. More detailed analysis of Adora2b(loxP/loxP) SPC Cre(+) mice confirmed elevated lung inflammation and attenuated alveolar fluid clearance. To directly deliver an A2B adenosine receptor-specific agonist to alveolar epithelial cells, we subsequently performed studies with inhaled BAY 60-6583. Indeed, aerosolized BAY 60-6583 treatment was associated with attenuated pulmonary edema, improved histologic lung injury, and dampened lung inflammation. Collectively, these findings suggest that alveolar epithelial A2B adenosine receptor signaling contributes to lung protection, and they implicate inhaled A2B adenosine receptor agonists in ALI treatment.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401957
Journal	The Journal of Immunology
Issue Number	4
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-08-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute Lung Injury Metabolism Pneumocytes Receptor, Adenosine A2b Drug Therapy Genetics Pathology Adenosine A2 Receptor Agonists Administration & Dosage Administration, Inhalation Animals Disease Models, Animal Gene Deletion Genetic Predisposition To Disease Macrophages, Alveolar Mice Mice, Knockout Neutrophils Organ Specificity Severity Of Illness Index Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Adenosine A2b receptors control A1 receptor-mediated inhibition of synaptic transmission in the mouse hippocampus.

TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury.

Alveolar Epithelial A2B Adenosine Receptors in Pulmonary Protection during Acute Lung Injury.

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