ArticleJournal of leukocyte biology2008
Preconditioning with high mobility group box 1 (HMGB1) induces lipopolysaccharide (LPS) tolerance.
Article in Journal of leukocyte biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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.
The trial behind it
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
38 citing papers in PubMed, 73 citations in OpenAlex.
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
- Damage-associated molecular patterns (DAMPs) in diseases: implications for therapy.Molecular biomedicine · 2025Review
- DAMP-driven trained immunity: metabolic and epigenetic reprogramming in critical illness and chronic inflammation.Frontiers in immunology · 2025Review
- Severe thermal and major traumatic injury results in elevated plasma concentrations of total heme that are associated with poor clinical outcomes and systemic immune suppression.Frontiers in immunology · 2024Article
- Role of gut microbiota in the modulation of the health effects of advanced glycation end‑products (Review).International journal of molecular medicine · 2023Review
- The immune suppressive properties of damage associated molecular patterns in the setting of sterile traumatic injury.Frontiers in immunology · 2023Review
- Review
- LPS Primes Brain Responsiveness to High Mobility Group Box-1 Protein.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Paeonol attenuates inflammation by confining HMGB1 to the nucleus.Journal of cellular and molecular medicine · 2021Article
- Endothelial Senescence and Chronic Fatigue Syndrome, a COVID-19 Based Hypothesis.Frontiers in cellular neuroscience · 2021Article
- HMGB1/TLR4 Signaling Affects Regulatory T Cells in Acute Lung Injury.Journal of inflammation research · 2021Article
- The role of RAGE in host pathology and crosstalk between RAGE and TLR4 in innate immune signal transduction pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Synergy between 15-lipoxygenase and secreted PLAProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Trained immunity as a molecular mechanism for BCG immunotherapy in bladder cancer.Nature reviews. Urology · 2020Review
- Identification of tetranectin-targeting monoclonal antibodies to treat potentially lethal sepsis.Science translational medicine · 2020Article
- Extracellular CIRP induces macrophage endotoxin tolerance through IL-6R-mediated STAT3 activation.JCI insight · 2020Article
- Targeting Inflammation Driven by HMGB1.Frontiers in immunology · 2020Review
- Time to Develop Therapeutic Antibodies Against Harmless Proteins Colluding with Sepsis Mediators?ImmunoTargets and therapy · 2020Review
- Damage- and pathogen-associated molecular patterns play differential roles in late mortality after critical illness.JCI insight · 2019Article
- Glucocorticoid receptor promotes the function of myeloid-derived suppressor cells by suppressing HIF1α-dependent glycolysis.Cellular & molecular immunology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
High mobility group box protein 1 (HMGB1) modulates the innate immune response when present in the extracellular compartment. Receptors for HMGB1 include TLR4, TLR2, and the receptor for advanced glycation end products (RAGE). We tested the hypothesis that extracellular HMGB1 can induce LPS tolerance. HMGB1 dose-response experiments were performed on IFN-gamma-differentiated human monocyte-like THP-1 cells. Treatment with 1 microg/ml HMGB1 18 h before exposure to LPS (1 microg/ml) decreased TNF release, NF-kappaB nuclear DNA-binding activity, phosphorylation, and degradation of IkappaBalpha. Preconditioning with HMGB1 alone and HMGB1 in the presence of polymyxin B decreased LPS-mediated, NF-kappaB-dependent luciferase reporter gene expression. The specificity of HMGB1 in tolerance induction was supported further by showing that boiled HMGB1 failed to induce tolerance, and antibodies against HMGB1 blocked the induction of LPS tolerance. Bone marrow-derived macrophages obtained from C57Bl/6 wild-type mice became LPS-tolerant following HMGB1 exposure ex vivo, but macrophages derived from RAGE-deficient mice failed to develop tolerance and responded normally to LPS. Mice preconditioned with HMGB1 (20 microg) 1 h before LPS injection (10 mg/kg) had lower circulating TNF compared with control mice preconditioned with saline vehicle. Similarly, decreased nuclear DNA binding of hepatic NF-kappaB was observed in mice preconditioned with HMGB1. Taken together, these results suggest that extracellular HMGB1 induces LPS tolerance, and the RAGE receptor is required for this induction.
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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.