Blockage of P2X7 attenuates acute lung injury in mice by inhibiting NLRP3 inflammasome
Open accessAbstract
NLRP3 inflammasome is engaged in the inflammatory response during acute lung injury (ALI). Purinergic receptor P2X7 has been reported to be upstream of NLRP3 activation. However, the therapeutic implication of P2X7 in ALI remains to be explored. The present study used lipopolysaccharide (LPS)-induced mouse model to investigate the therapeutic potential of P2X7 blockage in ALI. Our results showed that P2X7/NLRP3 inflammasome pathway was significantly upregulated in the lungs of ALI mice as compared with control mice. P2X7 antagonist A438079 suppressed NLRP3/ASC/caspase 1 activation, production of IL-1β, IL-17A and IFN-γ and neutrophil infiltration but not the production of IL-10, resulting in a significant amelioration of lung injury. Moreover, blockage of P2X7 significantly inhibited NLRP3 inflammasome activation and IL-1β production in bone marrow derived macrophages. Similar results were obtained using another P2X7 inhibitor brilliant blue G (BBG) in vivo. Thus, pharmacological blockage of P2X7/NLRP3 pathway can be considered as a potential therapeutic strategy in patients with ALI.
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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 [90]
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References 43 · Cited by 68
- Authors
- Wang, S., Zhao, J., Wang, H., Liang, Y., Yang, N., & Huang, Y.
- Affiliations
- Sun Yat-sen University (CN)
- Corresponding author
- Huang, Yuefang
- Venue
- International Immunopharmacology
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 27
- Issue
- 1
- Pages
- 38-45
- ISSN
- 1567-5769 (ISSN-L)
- PMC
- PMC7185518
- OpenAlex
- W2038510554
- Cited by
- 68
- References
- 43
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 7 · 2023: 9 · 2022: 5 · 2021: 5 · 2020: 7 · 2019: 7 · 2018: 8 · 2017: 5 · 2016: 6 · 2015: 1
- FWCI
- 2.90
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- International Immunopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Guangzhou Municipal Science and Technology Project (2012J4100085)
- National Natural Science Foundation of China (81273278, 81471598)
- Ministry of Education of the People's Republic of China (20120171110064)
- Natural Science Foundation of Guangdong Province (S2011010004578, S2012010008780)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- P2X7 receptor, NLRP3 inflammasome, acute lung injury, A438079, Brilliant Blue G, lipopolysaccharide-induced lung injury, IL-1β, caspase-1, ASC, neutrophil infiltration, macrophages, purinergic signaling, anti-inflammatory therapy
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Disease Models, Animal, Humans, Lipopolysaccharides, Macrophages, Male, Mice, Inbred C57BL, Neutrophils, Pyridines, Tetrazoles, Cytokines, Mice, Acute Lung Injury, Receptors, Purinergic P2X7, Inflammasomes, Purinergic P2X Receptor Antagonists
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