ArticleInfection and immunity2012
Contribution of adenosine A(2B) receptors in Clostridium difficile intoxication and infection.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Fatal Systemic Infection Caused by Multidrug-ResistantAntibiotics (Basel, Switzerland) · 2026Article
- Damage response signaling by the extracellular adenosine pathway: control of infection outcome during host aging.mSphere · 2025Review
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Clostridioides difficile meets the adenosine system: the art of manipulating host homeostasis.Journal of biomedical science · 2025Review
- Clostridioides difficile infection promotes gastrointestinal dysfunction in human and mice post-acute phase of the disease.Anaerobe · 2024Article
- Cupping alleviates lung injury through the adenosine/AHeliyon · 2022Article
- Mitochondrial ROS production by neutrophils is required for host antimicrobial function against Streptococcus pneumoniae and is controlled by A2B adenosine receptor signaling.PLoS pathogens · 2022Article
- Adenosine receptors differentially mediate enteric glial cell death induced byFrontiers in immunology · 2022Article
- Clostridium difficile toxins or infection induce upregulation of adenosine receptors and IL-6 with early pro-inflammatory and late anti-inflammatory pattern.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Blood-Brain Barrier in a Haemophilus influenzae Type a In Vitro Infection: Role of Adenosine Receptors AMolecular neurobiology · 2018Article
- Unfolding Role of a Danger Molecule Adenosine Signaling in Modulation of Microbial Infection and Host Cell Response.International journal of molecular sciences · 2018Review
- Adenosine AJournal of clinical medicine · 2017Review
- Intestinal Epithelial Ecto-5'-Nucleotidase (CD73) Regulates Intestinal Colonization and Infection by Nontyphoidal Salmonella.Infection and immunity · 2017Article
- Asymptomatic Clostridium difficile colonization: epidemiology and clinical implications.BMC infectious diseases · 2015Review
- Ecto-5'-nucleotidase (CD73) regulates host inflammatory responses and exacerbates murine salmonellosis.Scientific reports · 2014Article
- Adenosine and gastrointestinal inflammation.Journal of molecular medicine (Berlin, Germany) · 2013Review
- Adenosine A2A receptor activation reduces recurrence and mortality from Clostridium difficile infection in mice following vancomycin treatment.BMC infectious diseases · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Clostridium difficile toxins A (TcdA) and B (TcdB) induce a pronounced systemic and intestinal inflammatory response. A(2B) adenosine receptors (A(2B)ARs) are the predominant adenosine receptors in the intestinal epithelium. We investigated whether A(2B)ARs are upregulated in human intestinal cells by TcdA or TcdB and whether blockade of A(2B)ARs can ameliorate C. difficile TcdA-induced enteritis and alter the outcome of C. difficile infection (CDI). Adenosine receptor subtype (A(1), A(2A), A(2B), and A(3)) mRNAs were assayed in HCT-8 cells. Ileal loops from wild-type rabbits and mice and A(2B)AR(-/-) mice were treated with TcdA, with or without the selective A(2B)AR antagonist ATL692 or PSB1115. A murine model of CDI was used to determine the effect of A(2B)AR deletion or blockade with the orally available agent ATL801, on clinical outcome, histopathology and intestinal interleukin-6 (IL-6) expression from infection. TcdA and TcdB upregulated A(2B)AR gene expression in HCT-8 cells. ATL692 decreased TcdA-induced secretion and epithelial injury in rabbit ileum. Deletion of A(2B)ARs reduced secretion and histopathology in TcdA-challenged mouse ileum. Deletion or blockade of A(2B)ARs reduced histopathology, IL-6 expression, weight loss, diarrhea, and mortality in C. difficile-infected mice. A(2B)ARs mediate C. difficile toxin-induced enteritis and disease. Inhibition of A(2B)AR activation may be a potential strategy to limit morbidity and mortality from CDI.
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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.