ArticleInternational journal of biological sciences2023
PD-L1 promotes GSDMD-mediated NET release by maintaining the transcriptional activity of Stat3 in sepsis-associated encephalopathy.
Article in International journal of biological sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- ERK/Smurf1 regulates non-canonical pyroptosis by prompting Caspase-11 ubiquitination.Cell death and differentiation · 2026Article
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- ProteinJournal of pharmaceutical analysis · 2026Review
- Neuroimmune Mechanisms Transforming Acute Injury to Long-Term Brain Dysfunction After Sepsis.Clinics in chest medicine · 2026Review
- Intracellular PD-L1: Functions, Regulation, and Therapeutic Implications.International journal of biological sciences · 2026Review
- Propofol decreases the resistance of neutrophils to Candida albicans by inhibiting ferroptosis and the cGAS-STING pathway.American journal of translational research · 2026Article
- Gasdermin D-driven pyroptosis in sepsis: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- Molecular hydrogen-mediated SIRT1 activation alleviates sepsis-associated encephalopathy by promoting mitophagy.European journal of medical research · 2025Article
- Prevalence, symptoms, risk factors and impact of sepsis-associated encephalopathy in emergency department patients: a case-control study.BMC emergency medicine · 2025Article
- NIF inhibits the ability of PMNs to produce inflammatory cytokines and reactive oxygen species in response toMicrobiology spectrum · 2025Article
- Delaying pyroptosis with an AI-screened gasdermin D pore blocker mitigates inflammatory response.Nature immunology · 2025Article
- Dimethyl fumarate improves sepsis-induced acute lung injury by inhibiting STING-mediated ferroptosis.Journal of bioenergetics and biomembranes · 2025Article
- Bacteroides Fragilis-Derived Outer Membrane Vesicles Deliver MiR-5119 and Alleviate Colitis by Targeting PD-L1 to Inhibit GSDMD-Mediated Neutrophil Extracellular Trap Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling NETs in Sepsis: From Cellular Mechanisms to Clinical Relevance.International journal of molecular sciences · 2025Review
- Neutrophils: a new target for postoperative cognitive dysfunction.Apoptosis : an international journal on programmed cell death · 2025Review
- Inhibition of neutrophil extracellular traps alleviates blood-brain barrier disruption and cognitive dysfunction via Wnt3/β-catenin/TCF4 signaling in sepsis-associated encephalopathy.Journal of neuroinflammation · 2025Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated encephalopathy (SAE), as shown as acute and long-term cognitive impairment, is associated with increased mortality of sepsis. The causative factors of SAE are diverse and the underlying pathological mechanisms of SAE remain to be fully elucidated. Multiple studies have demonstrated a crucial role of microglia in the development of SAE, but the role of neutrophils and neutrophil extracellular traps (NETs) in SAE is still unclear. Here, we firstly show that in murine sepsis model, neutrophils and NETs promote blood-brain barrier (BBB) disruption, neuronal apoptosis and microglia activation in hippocampus and induce hippocampus-dependent memory impairment. Anti-Gr-1 antibody or DNase I treatment attenuates these sepsis-induced changes. Then, we find that genetic deletion of neutrophil GSDMD or PD-L1 reduces NET release and improves SAE in murine sepsis model. Finally, in human septic neutrophils, p-Y705-Stat3 binds to PD-L1, promotes PD-L1 nuclear translocation and enhances transcription of the gasdermin D (GSDMD) gene. In summary, our findings firstly identify a novel function of PD-L1 in maintaining transcriptional activity of p-Y705-Stat3 to promote GSDMD-dependent NET release in septic neutrophils, which plays a critical role in the development of SAE.
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