ReviewCritical care (London, England)2006
Bench-to-bedside review: endotoxin tolerance as a model of leukocyte reprogramming in sepsis.
Review in Critical care (London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
263 citing papers in PubMed, 470 citations in OpenAlex.
- Mitochondrial DAMPs induce endotoxin tolerance in human monocytes: an observation in patients with myocardial infarction.PloS one · 2014Trial
- Early Identification of a Cytokine-Low Immune Phenotype in Suspected Sepsis Using a Point-of-Care Whole-Blood TNF-α Release Assay.Medical sciences (Basel, Switzerland) · 2026Article
- From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Vagus nerve stimulation modulates LPS-induced epileptogenicity: the role of inflammation suppression.Research square · 2026Article
- Review
- The role of immunomodulatory nano systems in the treatment of sepsis: past, present, and future.Nanomedicine (London, England) · 2026Review
- From sepsis biomarker discovery to regulatedFrontiers in medical technology · 2026Review
- Early biomarkers for predicting sepsis-induced shock: insights from inflammatory pathways and immune response.Frontiers in pharmacology · 2026Review
- Point-of-care LPS-induced TNF-α release testing for early sepsis risk stratification in the emergency department.Frontiers in immunology · 2026Observational
- Recent advances in early screening and diagnosis of sepsis: a narrative review.Frontiers in cellular and infection microbiology · 2026Review
- Review
- Endotoxin's Impact on Organism: From Immune Activation to Tolerance and Beyond.Journal of clinical medicine · 2025Review
- Immunodynamic Disruption in Sepsis: Mechanisms and Strategies for Personalized Immunomodulation.Biomedicines · 2025Review
- Transcriptomic Profiling Reveals Distinct Immune Dysregulation in Early-Stage Sepsis Patients.International journal of molecular sciences · 2025Article
- Association between traumatic brain injury and risk of developing infections in the central nervous system and periphery.Metabolic brain disease · 2025Review
- Impaired Responses to In Vitro Lipopolysaccharide-Induced Stimulation After Long-Term, Rotating Shift Work.International journal of environmental research and public health · 2025Article
- Citrulline regulates macrophage metabolism and inflammation to counter aging in mice.Science advances · 2025Article
- FUNCTIONAL IMMUNOPHENOTYPING FOR PRECISION THERAPIES IN SEPSIS.Shock (Augusta, Ga.) · 2025Review
- Reassessing sepsis research: new clues for old players and new players for an old symptom to improve patient outcomes.EXCLI journal · 2025Review
- Identification and validation of an endotoxin tolerance-based prognostic model with therapeutic insights in sepsis.Frontiers in immunology · 2025Article
203 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endotoxin tolerance is defined as a reduced responsiveness to a lipopolysaccharide (LPS) challenge following a first encounter with endotoxin. Endotoxin tolerance protects against a lethal challenge of LPS and prevents infection and ischemia-reperfusion damage. Endotoxin tolerance is paralleled by a dramatic reduction of tumor necrosis factor (TNF) production and some other cytokines in response to LPS. Endotoxin tolerance involves the participation of macrophages and mediators, such as glucocorticoids, prostaglandins, IL-10, and transforming growth factor-beta. Endotoxin tolerance is accompanied by the up-regulation of inhibitory molecules that down-regulate the Toll-like receptor (TLR)4-dependent signaling pathway. Cross-tolerance between LPS and other TLR specific ligands, as well as IL-1 and TNF, has been regularly reported. A similar loss of LPS reactivity has been repeatedly reported in circulating leukocytes of septic patients and in patients with non-infectious systemic inflammation response syndrome (SIRS). Studies on cellular signaling within leukocytes from septic and SIRS patients reveal numerous alterations reminiscent of those observed in endotoxin tolerant cells. However, altered responsiveness to LPS of leukocytes from sepsis and SIRS patients is not synonymous with a global down-regulation of cellular reactivity. The term 'cellular reprogramming', which has been proposed to qualify the process of endotoxin tolerance, defines well the immune status of circulating leukocytes in septic and SIRS patients.
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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.