ArticleJournal of immunology research2017
Adenosine Triphosphate Promotes Allergen-Induced Airway Inflammation and Th17 Cell Polarization in Neutrophilic Asthma.
Article in Journal of immunology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Review
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- Calcium Signaling in Airway Epithelial Cells: Current Understanding and Implications for Inflammatory Airway Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Bioinformatic analysis and experimental validation of the potential gene in the airway inflammation of steroid-resistant asthma.Scientific reports · 2023Article
- Desert particulate matter from Afghanistan increases airway obstruction in human distal lungs exposed to type 2 cytokine IL-13.Frontiers in medicine · 2023Article
- Extracellular Nucleotides and Histamine Suppress TLR3- and RIG-I-Mediated Release of Antiviral IFNs from Human Airway Epithelial Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Chronic allergy signaling: is it all stressed-out mitochondria?Faculty reviews · 2022Review
- Differential Regulation of ATP- and UTP-Evoked Prostaglandin EJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Novel Pathway of Adenosine Generation in the Lungs from NADMolecules (Basel, Switzerland) · 2020Article
- Blocking pannexin1 reduces airway inflammation in a murine model of asthma.American journal of translational research · 2020Article
- Allergic sensitization increases the amount of extracellular ATP hydrolyzed by guinea pig leukocytes.Purinergic signalling · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenosine triphosphate (ATP) is a key mediator to alert the immune dysfunction by acting on P2 receptors. Here, we found that allergen challenge caused an increase of ATP secretion in a murine model of neutrophilic asthma, which correlated well with neutrophil counts and interleukin-17 production. When ATP signaling was blocked by intratracheal administration of the ATP receptor antagonist suramin before challenge, neutrophilic airway inflammation, airway hyperresponsiveness, and Th17-type responses were reduced significantly. Also, neutrophilic inflammation was abrogated when airway ATP levels were locally neutralized using apyrase. Furthermore, ATP promoted the Th17 polarization of splenic CD4
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