ArticleMediators of inflammation2015
ROS-Mediated NLRP3 Inflammasome Activity Is Essential for Burn-Induced Acute Lung Injury.
Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 84 citations in OpenAlex.
- The regulation of oxidative stress response by epigenetic modifications in acute respiratory distress syndrome.Journal of thoracic disease · 2026Review
- Omega-3 PUFAs Mitigate Polytrauma-Induced Gut-Liver-Lung Inflammation and Organ Dysfunction via GPR120/PPAR-γ.Journal of inflammation research · 2026Article
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- Low-pressure exposure influences the development of HAPE.Open life sciences · 2025Article
- Asiaticoside alleviates lipopolysaccharide-induced acute lung injury by blocking Sema4D/CD72 and inhibiting mitochondrial dysfunction in RAW264.7 cell and mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The NLRP3 inflammasome in burns: a novel potential therapeutic target.Burns & trauma · 2024Review
- Protective Effects of Sitagliptin on Streptozotocin-Induced Hepatic Injury in Diabetic Rats: A Possible Mechanisms.Diseases (Basel, Switzerland) · 2023Article
- Prdx6 Regulates Nlrp3 Inflammasome Activation-Driven Inflammatory Response in Lens Epithelial Cells.International journal of molecular sciences · 2023Article
- Effect of Hydrogen on AM Pyroptosis Induced by Severe Burns in Rats.Journal of personalized medicine · 2023Article
- Receptor for Advanced Glycation End-Products Promotes Activation of Alveolar Macrophages through the NLRP3 Inflammasome/TXNIP Axis in Acute Lung Injury.International journal of molecular sciences · 2022Article
- Citrulline protects against LPS‑induced acute lung injury by inhibiting ROS/NLRP3‑dependent pyroptosis and apoptosis via the Nrf2 signaling pathway.Experimental and therapeutic medicine · 2022Article
- The pro-inflammatory effect of Staphylokinase contributes to community-associated Staphylococcus aureus pneumonia.Communications biology · 2022Article
- Alleviation of chemotherapy-induced acute lung injury via NLRP3/ ASC/ Caspase-1 signaling pathway.Toxicology research · 2022Article
- Innate Immune System Response to Burn Damage-Focus on Cytokine Alteration.International journal of molecular sciences · 2022Review
- Article
- Antioxidant mitoquinone ameliorates EtOH-LPS induced lung injury by inhibiting mitophagy and NLRP3 inflammasome activation.Frontiers in immunology · 2022Article
- The Notch pathway attenuates burn-induced acute lung injury in rats by repressing reactive oxygen species.Burns & trauma · 2022Article
- NLRP3 Knockout Protects against Lung Injury Induced by Cerebral Ischemia-Reperfusion.Oxidative medicine and cellular longevity · 2022Article
- Immunomonitoring of Monocyte and Neutrophil Function in Critically Ill Patients: From Sepsis and/or Trauma to COVID-19.Journal of clinical medicine · 2021Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRP3 inflammasome is necessary for initiating acute sterile inflammation. However, its role in the pathogenesis of burn-induced acute lung injury (ALI) is unknown. This study aimed to determine the role of the NLRP3 inflammasome and the signaling pathways involved in burn-induced ALI. We observed that the rat lungs exhibited enhanced inflammasome activity after burn, as evidenced by increased levels of NLRP3 expression and Caspase-1 activity and augmented inflammatory cytokines. Inhibition of NLRP3 inflammasome by BAY11-7082 attenuated burn-induced ALI, as demonstrated by the concomitant remission of histopathologic changes and the reduction of myeloperoxidase (MPO) activity, inflammatory cytokines in rat lung tissue, and protein concentrations in the bronchoalveolar lavage fluid (BALF). In the in vitro experiments, we used AMs (alveolar macrophages) challenged with burn serum to mimic the postburn microenvironment and noted that the serum significantly upregulated NLRP3 inflammasome signaling and reactive oxygen species (ROS) production. The use of ROS scavenger N-acetylcysteine (NAC) partially reversed NLRP3 inflammasome activity in cells exposed to burn serum. These results indicate that the NLRP3 inflammasome plays an essential role in burn-induced ALI and that burn-induced NLRP3 inflammasome activity is a partly ROS-dependent process. Targeting this axis may represent a promising therapeutic strategy for the treatment of burn-induced ALI.
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