Extracellular ATP Is a Danger Signal Activating P2X7 Receptor in Lung Inflammation and Fibrosis
Abstract
Rationale: Pulmonary fibrosis is a devastating as yet untreatable disease. We previously investigated the endogenous mediators released on lung injury and showed that uric acid is a danger signal activating Nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome in lung inflammation and fibrosis (Gasse et al., Am J Respir Crit Care Med 2009;179:903–913). Objectives: Here we address the role of extracellular adenosine triphosphate (eATP) in pulmonary inflammation and fibrosis. Methods: ATP was quantified in bronchoalveolar lavage fluid (BALF) of control subjects and patients with idiopathic pulmonary fibrosis. The contribution of eATP as a danger signal was assessed in a murine model of lung fibrosis induced by airway-administered bleomycin (BLM), an intercalating agent that causes DNA strand breaks. Measurements and Main Results: Fibrotic patients have elevated ATP content in BALF in comparison with control individuals. In mice, we report an early increase in eATP levels in BALF on BLM administration. Modulation of eATP levels with the ATP-degrading enzyme apyrase greatly reduced BLM-induced inflammatory cell recruitment, lung IL-1β, and tissue inhibitor of metalloproteinase (TIMP)-1 production, while administration of ATP-γS, a stable ATP derivative, enhanced inflammation. P2X7 receptor–deficient mice presented dramatically reduced lung inflammation, with reduced fibrosis markers such as lung collagen content and matrix-remodeling proteins TIMP-1 and matrix metalloproteinase-9. The acute inflammation depends on a functional pannexin-1 hemichannel protein. In vitro, ATP is released by pulmonary epithelial cells on BLM-induced stress and this is partly dependent on the presence of functional P2X7 receptor and pannexin-1 hemichannel. Conclusions: ATP released from BLM-injured lung cells constitutes a major endogenous danger signal that engages the P2X7 receptor/pannexin-1 axis, leading to IL-1β maturation and lung fibrosis.
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P2X7 receptor expression deletion appears to be beneficial in acute lung injury, asthma, lung inflammation, and fibrosis.
“In addition, P2X7 receptor expression deletion appears to be beneficial in case of acute lung injury, asthma, lung inflammation, and fibrosis [87–91].”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [89]
Inhibition of the P2X7 receptor might decrease pathological traits mediated by the RAAS pressor axis and protect against brain and lung injury in COVID-19 patients.
“Since the P2X7 receptor is also involved in lung damage [87–89], neurodegenerative and psychiatric disorders [92, 95, 118], the hypothesis is reasonable that inhibition of this receptor might decrease pathological traits mediated by the RAAS pressor axis and protect against brain and lung injury in COVID-19 patients.”
From Hyperactivation of P2X7 receptors as a culprit of COVID-19 neuropathology (2021) · cites this paper as [89]
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- Authors
- Riteau, N., Gasse, P., Fauconnier, L., Gombault, A., Couegnat, M., Fick, L., Kanellopoulos, J., Quesniaux, V. F. J., Marchand-Adam, S., Crestani, B., Ryffel, B., & Couillin, I.
- Affiliations
- Université d'Orléans (FR)
- University of Orleans and National Center for Scientific Research UMR6218, Molecular Immunology and Embryology, Orleans, France
- University of Cape Town (ZA)
- Centre National de la Recherche Scientifique (FR)
- Université de Tours (FR)
- Inserm (FR)
- Venue
- American Journal of Respiratory and Critical Care Medicine
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-09
- Volume
- 182
- Issue
- 6
- Pages
- 774-783
- ISSN
- 1073-449X (ISSN-L)
- 1535-4970
- OpenAlex
- W2167645193
- Cited by
- 397
- References
- 48
- Citations by year
- 2026: 8 · 2025: 20 · 2024: 16 · 2023: 29 · 2022: 19 · 2021: 28 · 2020: 26 · 2019: 17 · 2018: 40 · 2017: 30 · 2016: 32 · 2015: 24 · 2014: 33 · 2013: 29 · 2012: 24
- FWCI
- 16.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Respiratory and Critical Care Medicine (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Keywords
- extracellular ATP, P2X7 receptor, pulmonary fibrosis, lung inflammation, damage-associated molecular patterns, bleomycin-induced lung injury, IL-1β, TIMP-1, MMP-9, apyrase, bronchoalveolar lavage fluid, lung epithelial cells, extracellular nucleotides
- MeSH terms
- Adenosine Triphosphate, Animals, Bleomycin, Bronchoalveolar Lavage Fluid, Disease Models, Animal, Humans, Mice, Inbred C57BL, Pneumonia, Pulmonary Fibrosis, Signal Transduction, Case-Control Studies, Receptors, Purinergic P2, Mice, Lung Injury, Receptors, Purinergic P2X7
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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