ReviewJournal of innate immunity2021
Intracellular and Extracellular Lipopolysaccharide Signaling in Sepsis: Avenues for Novel Therapeutic Strategies.
Review in Journal of innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.
- Emerging trends and hotspots in intestinal microbiota research in sepsis: bibliometric analysis.Frontiers in medicine · 2024Pooled it
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Acinetobacter baumannii lipooligosaccharide core region promotes CD14-dependent TLR4 endocytosis and enhances pathogenicity through interferon-β production.PLoS pathogens · 2026Article
- Monoclonal Antibodies Targeting Bacterial Infections: A Broad Review of the Field.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026Review
- Ion channels and GPCRs as pharmacological regulators of ferroptosis and pyroptosis in metabolic diseases.Diabetology & metabolic syndrome · 2026Review
- Sepsis modelling: current approaches and organ-on-chip perspectives.EBioMedicine · 2026Review
- Endotoxins and Metabolic Endotoxemia in Obesity and Associated Noncommunicable Diseases: A Focus on Sex Differences.Biomolecules · 2026Review
- Virulence arsenal of Acinetobacter baumannii: mechanisms driving persistence and resistance.Archives of microbiology · 2026Review
- Increased Toll-Like Receptor-4 Signalling in Breast Tissue of High Fibroglandular Density.Journal of mammary gland biology and neoplasia · 2026Article
- Emestrin-Type Epidithiodiketopiperazines Inhibited Gasdermin D-Mediated Pyroptosis via Caspase-3/7 Activation.MedComm · 2026Article
- Variable progressive behavior ofFrontiers in immunology · 2026Article
- Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.Frontiers in immunology · 2026Review
- Design and evaluation of octopromycin-derived peptides as multifunctional antimicrobial agents against multidrug-resistant pathogens.Scientific reports · 2025Article
- Polyglutamic Acid as an Antiviral Agent: Mechanistic and Structural Insights.Pharmaceutics · 2025Review
- Exploring the Antimicrobial and Antiviral Properties of Cryptic Peptides from Human Fibrinogen.International journal of molecular sciences · 2025Article
- Exploring the therapeutic potential of recombinant bovine β-defensins for antimicrobial and anti-inflammatory functions in sepsis management.Veterinary research · 2025Article
- Supramolecular Detoxification Approach of Endotoxin Through Host-Guest Complexation by a Giant Macrocycle.Molecules (Basel, Switzerland) · 2025Article
- Carbon dots from purple sweet potato as a promising anti-inflammatory biomaterial for alleviating the LPS-induced inflammation in macrophages.Journal of nanobiotechnology · 2025Article
- In Silico Exploration of Natural Antioxidants for Sepsis Drug Discovery.Molecules (Basel, Switzerland) · 2025Article
18 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Sepsis is defined as organ dysfunction due to a dysregulated systemic host response to infection. During gram-negative bacterial infection and other acute illness such as absorption from the gut infection, lipopolysaccharide (LPS) is a major mediator in sepsis. LPS is able to trigger inflammation through both intracellular and extracellular pathways. Classical interactions between LPS and host cells first involve LPS binding to LPS binding protein (LBP), a carrier. The LPS-LBP complex then binds to a receptor complex including the CD14, MD2, and toll-like receptor 4 (TLR4) proteins, initiating a signal cascade which triggers the secretion of pro-inflammatory cytokines. However, it has been established that LPS is also internalized by macrophages and endothelial cells through TLR4-independent pathways. Once internalized, LPS is able to bind to the cytosolic receptors caspases-4/5 in humans and the homologous caspase-11 in mice. Bound caspases-4/5 oligomerize and trigger the assembly of the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 inflammasome followed by the activation of inflammatory caspase-1 resulting in subsequent release of interleukin-1β. Caspases-4/5 also activate the perforin gasdermin D and purinergic receptor P2X7, inducing cell lysis and pyroptosis. Pyroptosis is a notable source of inflammation and damage to the lung endothelial barrier during sepsis. Thus, inhibition of caspases-4/5/1 or downstream effectors to block intracellular LPS signaling may be a promising therapeutic approach in adjunction with neutralizing extracellular LPS for treatment of sepsis.
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What OpenQuestion holds
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.