Deletion of P2X7 attenuates hyperoxia-induced acute lung injury via inflammasome suppression
Open accessAbstract
Increasing evidence shows that hyperoxia is a serious complication of oxygen therapy in acutely ill patients that causes excessive production of free radicals leading to hyperoxia-induced acute lung injury (HALI). Our previous studies have shown that P2X7 receptor activation is required for inflammasome activation during HALI. However, the role of P2X7 in HALI is unclear. The main aim of this study was to determine the effect of P2X7 receptor gene deletion on HALI. Wild-type (WT) and P2X7 knockout (P2X7 KO) mice were exposed to 100% O 2 for 72 h. P2X7 KO mice treated with hyperoxia had enhanced survival in 100% O 2 compared with the WT mice. Hyperoxia-induced recruitment of inflammatory cells and elevation of IL-1β, TNF-α, monocyte chemoattractant protein-1, and IL-6 levels were attenuated in P2X7 KO mice. P2X7 deletion decreased lung edema and alveolar protein content, which are associated with enhanced alveolar fluid clearance. In addition, activation of the inflammasome was suppressed in P2X7-deficient alveolar macrophages and was associated with suppression of IL-1β release. Furthermore, P2X7-deficient alveolar macrophage in type II alveolar epithelial cells (AECs) coculture model abolished protein permeability across mouse type II AEC monolayers. Deletion of P2X7 does not lead to a decrease in epithelial sodium channel expression in cocultures of alveolar macrophages and type II AECs. Taken together, these findings show that deletion of P2X7 is a protective factor and therapeutic target for the amelioration of hyperoxia-induced lung injury.
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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 [87]
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 [87]
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- Authors
- Galam, L., Rajan, A., Failla, A., Soundararajan, R., Lockey, R. F., & Kolliputi, N.
- Affiliations
- University of South Florida (US)
- Corresponding author
- Kolliputi, Narasaiah
- Venue
- American Journal of Physiology-Lung Cellular and Molecular Physiology
- Publisher
- American Physiological Society
- Published
- 2016-03-15
- Volume
- 310
- Issue
- 6
- Pages
- L572-L581
- ISSN
- 1040-0605 (ISSN-L)
- 1522-1504
- PMC
- PMC4796258
- OpenAlex
- W2256438016
- Cited by
- 52
- References
- 68
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 5 · 2020: 6 · 2019: 7 · 2018: 7 · 2017: 7 · 2016: 4
- FWCI
- 7.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Lung Cellular and Molecular Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons - University of South Florida (University of South Florida) (submittedVersion)
- Funders
- NIH (R01 HL105932)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- P2X7 receptor, inflammasome, IL-1β, alveolar macrophages, alveolar type II cells, alveolar fluid clearance, epithelial permeability, epithelial sodium channel, inflammatory cytokines, pulmonary edema, oxygen therapy complications
- MeSH terms
- Animals, Cells, Cultured, Female, Male, Membrane Potentials, Mice, Inbred C57BL, Lipid Peroxidation, Mice, Knockout, Hyperoxia, Coculture Techniques, Caspase 1, Neutrophil Infiltration, Interleukin-1beta, Acute Lung Injury, Alveolar Epithelial Cells, Receptors, Purinergic P2X7, Inflammasomes, Protective Factors
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