ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
CD39 improves survival in microbial sepsis by attenuating systemic inflammation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 67 citations in OpenAlex.
- CD39 regulates P2RX7-mediated lung necrotic lesions in severe experimental tuberculosis.Mucosal immunology · 2026Article
- Article
- Nucleotide Metabolic Reprogramming in Sepsis: From Immune-Cell Fate to Organ Injury and Precision Therapeutics.Journal of inflammation research · 2026Review
- CD39 and CD73: biological functions, diseases and therapy.Molecular biomedicine · 2025Review
- Integrating bioinformatics and machine learning to discover sumoylation associated signatures in sepsis.Scientific reports · 2025Article
- Shenfu injection alleviates lipopolysaccharide-induced liver injury in septic mice.Scientific reports · 2025Article
- Causal effects of circulating immune cells on coronary atherosclerosis: Evidence from Mendelian randomization.Medicine · 2025Article
- Anti-DAMP therapies for acute inflammation.Frontiers in immunology · 2025Review
- Adenosine Triphosphate Release From Influenza-Infected Lungs Enhances Neutrophil Activation and Promotes Disease Progression.The Journal of infectious diseases · 2024Article
- Upregulation of CD39 During Gout Attacks Promotes Spontaneous Remission of Acute Gouty Inflammation.Inflammation · 2024Article
- Platelet P2YBritish journal of pharmacology · 2024Review
- Sagittal Abdominal Diameter as the Best Predictor of Metabolic Syndrome in HIV-Infected Men on Antiretroviral Therapy.Current HIV research · 2024Article
- ATPergic signaling disruption in human sepsis as a potential source of biomarkers for clinical use.Clinical and experimental medicine · 2023Article
- P2Y2 purinergic receptor gene deletion protects mice from bacterial endotoxin and sepsis-associated liver injury and mortality.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- APurinergic signalling · 2022Article
- P2X receptors in the balance between inflammation and pathogen control in sepsis.Purinergic signalling · 2022Article
- Ginkgolic acid promotes inflammation and macrophage apoptosisFrontiers in medicine · 2022Article
- Extracellular ectonucleotidases are differentially regulated in murine tissues and human polymorphonuclear leukocytes during sepsis and inflammation.Purinergic signalling · 2021Article
- Inosine monophosphate and inosine differentially regulate endotoxemia and bacterial sepsis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Thrombo-Inflammation: A Focus on NTPDase1/CD39.Cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Sepsis remains the leading cause of morbidity and mortality in critically ill patients. Excessive inflammation is a major cause of organ failure and mortality in sepsis. Ectonucleoside triphosphate diphosphohydrolase 1, ENTPDase1 (CD39) is a cell surface nucleotide-metabolizing enzyme, which degrades the extracellular purines ATP and ADP, thereby regulating purinergic receptor signaling. Although the role of purinergic receptor signaling in regulating inflammation and sepsis has been addressed previously, the role of CD39 in regulating the host's response to sepsis is unknown. We found that the CD39 mimic apyrase (250 U/kg) decreased and knockout or pharmacologic blockade with sodium polyoxotungstate (5 mg/kg; IC50 ≈ 10 μM) of CD39 increased mortality of mice with polymicrobial sepsis induced by cecal ligation and puncture. CD39 decreased inflammation, organ damage, immune cell apoptosis, and bacterial load. Use of bone marrow chimeric mice revealed that CD39 expression on myeloid cells decreases inflammation in septic mice. CD39 expression is upregulated during sepsis in mice, as well as in both murine and human macrophages stimulated with Escherichia coli. Moreover, E. coli increases CD39 promoter activity in macrophages. Altogether, these data indicate CD39 as an evolutionarily conserved inducible protective pathway during sepsis. We propose CD39 as a novel therapeutic target in the management of sepsis.
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.