ReviewJournal of inflammation research2024
Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome.
Review in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- SPLUNC1/BPIFA1 Restrains Neutrophil-Dominant Inflammation and Coordinated Inflammatory Gene Programs During LPS-Induced Lung Injury.Biomolecules · 2026Article
- Article
- USP43-mediated deubiquitination of SLC7A11 protects against LPS-induced acute lung injury by inhibiting ferroptosis.Clinical and translational medicine · 2026Article
- Alveolar epithelial barrier disruption by FKBP5-mediated necroptosis aggravates lung injury.Respiratory research · 2026Article
- An immune-mediated effect of the antibiotic cefiderocol on LPS-induced acute lung injury.Antimicrobial agents and chemotherapy · 2026Article
- Investigating the role of miR-192-5p as a diagnostic biomarker and the anti-inflammatory function in pediatric acute respiratory distress syndrome.BMC immunology · 2026Article
- Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026Review
- Inhibition of S100A12 Attenuates LPS-induced Endothelial Barrier Dysfunction in HPMECs through the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Roll with the punches: Fibroblast growth factor 10 alleviates pyroptosis of alveolar epithelial cells in different immune niches.Clinical and translational medicine · 2026Article
- Melatonin Suppresses NLRP3 Inflammasome Activation via SIRT1-Mediated ETS1 Deacetylation to Attenuate LPS-Induced Pyroptosis in Alveolar Epithelial Cells.Journal of inflammation research · 2026Article
- Investigating the impact of selegiline on the NF-kB/NLRP3/Caspase-1 signaling pathway in A549 lung epithelial cells exposed to lipopolysaccharide.Cytotechnology · 2025Article
- Article
- Protective Effects of Pasireotide in LPS-Induced Acute Lung Injury.Pharmaceuticals (Basel, Switzerland) · 2025Article
- YTHDF1-mediated m6A modification of GBP4 promotes M1 macrophage polarization in acute lung injury.Respiratory research · 2025Article
- Plasma polymeric immunoglobulin receptor exacerbates lung injury inFrontiers in immunology · 2025Article
- Chaihuang Qingfu Pills Protect Against Acute Pancreatitis-Associated Acute Lung Injury Through MMP9-NLRP3-Pyroptosis Pathway.Journal of inflammation research · 2025Article
- Cornuside mitigates acute lung injury through suppression of NLRP3 inflammasome-mediated pyroptosis and activation of the Keap1-Nrf2 antioxidant response.Frontiers in pharmacology · 2025Article
- Regulation of Histone Acetylation During Inflammation Resolution.ImmunoTargets and therapy · 2025Article
- New Exploration of Therapeutic Targets for Radiation Pneumonitis: Comparative Analysis of Molecular Pathways in Radiation-Induced and LPS-Induced Pneumonitis.International journal of medical sciences · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a spectrum of common critical respiratory conditions characterized by damage and death of alveolar epithelial cells (AECs). Pyroptosis is a form of programmed cell death with inflammatory characteristics, and activation of pyroptosis markers has been observed in AECs of patients with ALI/ARDS. Lipopolysaccharides (LPS) possess strong pro-inflammatory effects and are a crucial pathological factor leading to ALI in patients and animals. In LPS-induced ALI models, AECs undergo pyroptosis. However, physiologically and pathologically relevant concentrations of LPS lead to minor effects on AEC cell viability and minimal induction of cytokine release in vitro and do not induce classical pyroptosis. Nevertheless, LPS can enter the cytoplasm directly and induce non-classical pyroptosis in AECs when assisted by extracellular vesicles from bacteria, HMGB1, and pathogens. In this review, we have explored the effects of LPS on AECs concerning inflammation, cell viability, and pyroptosis, analyzing key factors that influence LPS actions. Notably, we highlight the intricate response of AECs to LPS within the framework of ALI and ARDS, emphasizing the variable induction of pyroptosis. Despite the minimal effects of LPS on AEC viability and cytokine release in vitro, LPS can induce non-classical pyroptosis under specific conditions, presenting potential pathways for therapeutic intervention. Collectively, understanding these mechanisms is crucial for the development of targeted treatments that mitigate the inflammatory responses in ALI/ARDS, thereby enhancing patient outcomes in these severe respiratory conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.