ReviewFrontiers in immunology2020
Lipopolysaccharide Recognition in the Crossroads of TLR4 and Caspase-4/11 Mediated Inflammatory Pathways.
Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 150 papers.
What it found
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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
150 citing papers in PubMed, 191 citations in OpenAlex.
- RAGE mediates LPS-induced inflammatory pain in human skin - a double-blind, randomised, placebo-controlled full crossover study.Nature communications · 2026Trial
- Physical continuity at biomaterial-ECM interfaces is associated with reduced fibroblast activation and NF-κB signaling.Biomaterials · 2026Article
- Predicting resistance evolution to guide antibiotic development.Nature reviews. Microbiology · 2026Review
- Gut‑liver‑kidney axis: A systems biology framework for understanding and treating chronic kidney disease (Review).International journal of molecular medicine · 2026Review
- When folding CARDs wins the game: molecular snapshots of lipopolysaccharide sensing by the non-canonical inflammasome.Biochemical Society transactions · 2026Review
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- What goes around comes around: updates in the study ofInfection and immunity · 2026Review
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- Microbial Signals in Cancer: Dissecting Host-Microbiota-Tumor Interactions and Potential Therapeutic Strategy.MedComm · 2026Review
- PPE57 Cooperates with MmpL3 to Mediate Bacterial Lipid Transport and Promote Persistent Infection ofMicroorganisms · 2026Article
- Article
- Higher Lipopolysaccharide Levels Are Linked to Less Anhedonia and Lower Severity of Major Depressive Disorder.Brain sciences · 2026Article
- Phosphoethanolamine-modified lipid A enables antimicrobial resistance and atypical signaling properties in the marine pathogenMicrobiology spectrum · 2026Article
- Role and mechanism of quercetin via the TLR4/MyD88/IRAK4 signaling pathway in the treatment of allergic rhinitis.Experimental and therapeutic medicine · 2026Article
- Review
- How to recognize if a cell dies from pyroptosis?Molecular biology reports · 2026Review
- Experimental models for intestinal host-microbe interactions.EMBO molecular medicine · 2026Review
- Advances in understanding the NLRP3 inflammasome‑mediated mechanisms and therapeutic targets in diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- Presurgical immune biomarkers associated with pain intensity and pain interference recovery after total knee arthroplasty: findings from the PRIME-KNEE study.medRxiv : the preprint server for health sciences · 2026Article
- A novel two-hit murine model of viral-primed sepsis-associated acute kidney injury.American journal of physiology. Renal physiology · 2026Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The innate immune response to lipopolysaccharide is essential for host defense against Gram-negative bacteria. In response to bacterial infection, the TLR4/MD-2 complex that is expressed on the surface of macrophages, monocytes, dendritic, and epithelial cells senses picomolar concentrations of endotoxic LPS and triggers the production of various pro-inflammatory mediators. In addition, LPS from extracellular bacteria which is either endocytosed or transfected into the cytosol of host cells or cytosolic LPS produced by intracellular bacteria is recognized by cytosolic proteases caspase-4/11 and hosts guanylate binding proteins that are involved in the assembly and activation of the NLRP3 inflammasome. All these events result in the initiation of pro-inflammatory signaling cascades directed at bacterial eradication. However, TLR4-mediated signaling and caspase-4/11-induced pyroptosis are largely involved in the pathogenesis of chronic and acute inflammation. Both extra- and intracellular LPS receptors-TLR4/MD-2 complex and caspase-4/11, respectively-are able to directly bind the lipid A motif of LPS. Whereas the structural basis of lipid A recognition by the TLR4 complex is profoundly studied and well understood, the atomic mechanism of LPS/lipid A interaction with caspase-4/11 is largely unknown. Here we describe the LPS-induced TLR4 and caspase-4/11 mediated signaling pathways and their cross-talk and scrutinize specific structural features of the lipid A motif of diverse LPS variants that have been reported to activate caspase-4/11 or to induce caspase-4/11 mediated activation of NLRP3 inflammasome (either upon transfection of LPS
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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.