ArticleAmerican journal of respiratory cell and molecular biology2013
Macrophage A2A adenosinergic receptor modulates oxygen-induced augmentation of murine lung injury.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Comparative Transcriptomic Analysis of Human Macrophages During Mycobacterium avium Versus Mycobacterium tuberculosis Infection.Molecular microbiology · 2026Article
- Potential pharmaceuticals targeting neuroimmune interactions in treating acute lung injury.Clinical and translational medicine · 2024Review
- H3K27 tri-demethylase JMJD3 inhibits macrophage apoptosis by promoting ADORA2A in lipopolysaccharide-induced acute lung injury.Cell death discovery · 2022Article
- Therapeutic Targeting of Hypoxia-A2-Adenosinergic Pathway in COVID-19 Patients.Physiology (Bethesda, Md.) · 2022Article
- Efficacy and Effect of Inhaled Adenosine Treatment in Hospitalized COVID-19 Patients.Frontiers in immunology · 2021Article
- Case Report: Can Inhaled Adenosine Attenuate COVID-19?Frontiers in pharmacology · 2021Article
- Can Adenosine Fight COVID-19 Acute Respiratory Distress Syndrome?Journal of clinical medicine · 2020Review
- Hypoxia and HIF Signaling: One Axis with Divergent Effects.International journal of molecular sciences · 2020Review
- Therapeutic effects of adenosine in high flow 21% oxygen aereosol in patients with Covid19-pneumonia.PloS one · 2020Article
- Blockade of equilibrative nucleoside transporter 1/2 protects against Pseudomonas aeruginosa-induced acute lung injury and NLRP3 inflammasome activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Transcription factor-mediated signaling pathways' contribution to the pathology of acute lung injury and acute respiratory distress syndrome.American journal of translational research · 2020Article
- Purinergic Regulation of Neutrophil Function.Frontiers in immunology · 2018Review
- Low-Dose Oxygen Enhances Macrophage-Derived Bacterial Clearance following Cigarette Smoke Exposure.Journal of immunology research · 2016Article
- Hypoxia signaling during acute lung injury.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Review
- Systemic oxygenation weakens the hypoxia and hypoxia inducible factor 1α-dependent and extracellular adenosine-mediated tumor protection.Journal of molecular medicine (Berlin, Germany) · 2014Article
- Immunological priming requires regulatory T cells and IL-10-producing macrophages to accelerate resolution from severe lung inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Diverse macrophage populations mediate acute lung inflammation and resolution.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Hyperoxia exacerbates postnatal inflammation-induced lung injury in neonatal BRP-39 null mutant mice promoting the M1 macrophage phenotype.Mediators of inflammation · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Acute respiratory distress syndrome (ARDS) causes significant morbidity and mortality. Exacerbating factors increasing the risk of ARDS remain unknown. Supplemental oxygen is often necessary in both mild and severe lung disease. The potential effects of supplemental oxygen may include augmentation of lung inflammation by inhibiting anti-inflammatory pathways in alveolar macrophages. We sought to determine oxygen-derived effects on the anti-inflammatory A2A adenosinergic (ADORA2A) receptor in macrophages, and the role of the ADORA2A receptor in lung injury. Wild-type (WT) and ADORA2A(-/-) mice received intratracheal lipopolysaccharide (IT LPS), followed 12 hours later by continuous exposure to 21% oxygen (control mice) or 60% oxygen for 1 to 3 days. We measured the phenotypic endpoints of lung injury and the alveolar macrophage inflammatory state. We tested an ADORA2A-specific agonist, CGS-21680 hydrochloride, in LPS plus oxygen-exposed WT and ADORA2A(-/-) mice. We determined the specific effects of myeloid ADORA2A, using chimera experiments. Compared with WT mice, ADORA2A(-/-) mice exposed to IT LPS and 60% oxygen demonstrated significantly more histologic lung injury, alveolar neutrophils, and protein. Macrophages from ADORA2A(-/-) mice exposed to LPS plus oxygen expressed higher concentrations of proinflammatory cytokines and cosignaling molecules. CGS-21680 prevented the oxygen-induced augmentation of lung injury after LPS only in WT mice. Chimera experiments demonstrated that the transfer of WT but not ADORA2A(-/-) bone marrow cells into irradiated ADORA2A(-/-) mice reduced lung injury after LPS plus oxygen, demonstrating myeloid ADORA2A protection. ADORA2A is protective against lung injury after LPS and oxygen. Oxygen after LPS increases macrophage activation to augment lung injury by inhibiting the ADORA2A pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.