ArticleJournal of leukocyte biology2017
Frontline Science: HMGB1 induces neutrophil dysfunction in experimental sepsis and in patients who survive septic shock.
Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- Emodin Alleviates Sepsis-Induced Multiorgan Damage by Inhibiting NETosis through Targeting Neutrophils BCL-10.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- sTREM-1, HMGB1, CRP, PCT, sCD14-ST, IL-6, IL-10, sHLA-G, and Vitamin D in Relation to Clinical Scores and Survival in SIRS/Sepsis.Biomedicines · 2025Article
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- Sepsis-induced immunosuppression: mechanisms, biomarkers and immunotherapy.Frontiers in immunology · 2025Review
- The progress of organ protection mechanisms in sepsis.Frontiers in immunology · 2025Review
- PAMPs and DAMPs in Sepsis: A Review of Their Molecular Features and Potential Clinical Implications.International journal of molecular sciences · 2024Review
- Fatal Clostridium septicum gas gangrene complicating ECMO: case report and review of literature.Access microbiology · 2024Article
- Ex Vivo Production of IL-1β and IL-10 by Activated Blood Cells of Wistar Rats with Different Resistance to Hypoxia after Systemic Inflammatory Response Syndrome.Bulletin of experimental biology and medicine · 2023Article
- HMGB1, angel or devil, in ischemic stroke.Brain and behavior · 2023Review
- Identification of procathepsin L (pCTS-L)-neutralizing monoclonal antibodies to treat potentially lethal sepsis.Science advances · 2023Article
- The Comprehensive Role of High Mobility Group Box 1 (HMGB1) Protein in Different Tumors: A Pan-Cancer Analysis.Journal of inflammation research · 2023Article
- The immune suppressive properties of damage associated molecular patterns in the setting of sterile traumatic injury.Frontiers in immunology · 2023Review
- Review
- HMGB1 is a critical molecule in the pathogenesis of Gram-negative sepsis.Journal of intensive medicine · 2022Review
- Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.Acta pharmacologica Sinica · 2022Review
- Beneficial effects of citrulline enteral administration on sepsis-induced T cell mitochondrial dysfunction.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- HMGB1: A Potential Target of Nervus Vagus Stimulation in Pediatric SARS-CoV-2-Induced ALI/ARDS.Frontiers in pediatrics · 2022Article
- Damage-Associated Molecular Patterns As Double-Edged Swords in Sepsis.Antioxidants & redox signaling · 2021Review
- ZKSCAN3 in severe bacterial lung infection and sepsis-induced immunosuppression.Laboratory investigation; a journal of technical methods and pathology · 2021Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Sepsis is accompanied by the initial activation of proinflammatory pathways and long-lasting immunosuppression that appears to contribute to late-occurring mortality. Although high-mobility group box 1 (HMGB1) is involved in many aspects of inflammation, its role in sepsis-induced immune suppression remains unclear. In this study, we examined HMGB1's contribution to neutrophil NADPH oxidase activity dysfunction and associated neutrophil-dependent bacterial clearance in mice subjected to sepsis and in patients who survive septic shock. Using a murine model of polymicrobial septic peritonitis, we demonstrated that treatment with anti-HMGB1 Ab significantly diminished sepsis-induced dysfunction of neutrophil NADPH oxidase activity. In a subsequent set of experiments, we found that blocking HMGB1 preserved the ability of neutrophils from patients recovering from septic shock to activate NADPH oxidase. Taken together, our data suggest that HMGB1 accumulation in the late phase of sepsis plays a specific role in the development of postsepsis immunosuppression and specifically affects neutrophil-dependent antibacterial defense mechanisms. Thus, blocking HMGB1 may be a promising therapeutic intervention to diminish the adverse effects of sepsis-induced immunosuppression.
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Registered trials
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.