ArticleMediators of inflammation2013
CD14 mediates binding of high doses of LPS but is dispensable for TNF-α production.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 50 citations in OpenAlex.
- Diacylglycerol kinase-ε is required for the formation of GPI-anchored CD14 and the LPS-induced proinflammatory responses of macrophages.Cell communication and signaling : CCS · 2026Article
- Dose-dependent effects of atorvastatin on inflammatory response in endothelial cells: MMP/TIMP balance and in vitro wound closure assay.BMC molecular and cell biology · 2026Article
- Erythrocyte membrane coated biodegradable nanoparticles detoxify LPS-induced toxicity by producing non-mutagenic metabolites and downregulating pro-inflammatory cytokines and oxidative stress markers.Scientific reports · 2025Article
- Article
- Flotillins affect LPS-induced TLR4 signaling by modulating the trafficking and abundance of CD14.Cellular and molecular life sciences : CMLS · 2024Article
- Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome.Journal of inflammation research · 2024Review
- Interplay between Systemic Glycemia and Neuroprotective Activity of Resveratrol in Modulating Astrocyte SIRT1 Response to Neuroinflammation.International journal of molecular sciences · 2023Article
- Target and Cell Therapy for Atherosclerosis and CVD.International journal of molecular sciences · 2023Review
- Dual Effect of the Extract from the FungusJournal of inflammation research · 2022Article
- Gut Microbiota Parameters Potentially Useful in Clinical Perspective.Microorganisms · 2021Review
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2021Review
- Article
- Lipopolysaccharide Preparation Derived FromFrontiers in cellular and infection microbiology · 2021Article
- Leptospiral LPS escapes mouse TLR4 internalization and TRIF‑associated antimicrobial responses through O antigen and associated lipoproteins.PLoS pathogens · 2020Article
- Lipopolysaccharide Upregulates Palmitoylated Enzymes of the Phosphatidylinositol Cycle: An Insight from Proteomic Studies.Molecular & cellular proteomics : MCP · 2018Article
- Lipopolysaccharide-induced inflammation in monocytes/macrophages is blocked by liposomal delivery of GInternational journal of nanomedicine · 2018Article
- Association of Lyn kinase with membrane rafts determines its negative influence on LPS-induced signaling.Molecular biology of the cell · 2017Article
- Secreted Thrombospondin-1 Regulates Macrophage Interleukin-1β Production and Activation through CD47.Scientific reports · 2016Article
- CD14 Is a Co-Receptor for TLR4 in the S100A9-Induced Pro-Inflammatory Response in Monocytes.PloS one · 2016Article
- Full Spectrum of LPS Activation in Alveolar Macrophages of Healthy Volunteers by Whole Transcriptomic Profiling.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of macrophages with lipopolysaccharide (LPS) involves a sequential engagement of serum LPS-binding protein (LBP), plasma membrane CD14, and TLR4/MD-2 signaling complex. We analyzed participation of CD14 in TNF-α production stimulated with 1-1000 ng/mL of smooth or rough LPS (sLPS or rLPS) and in sLPS binding to RAW264 and J744 cells. CD14 was indispensable for TNF-α generation induced by a low concentration, 1 ng/mL, of sLPS and rLPS. At higher doses of both LPS forms (100-1000 ng/mL), TNF-α release required CD14 to much lower extent. Among the two forms of LPS, rLPS-induced TNF-α production was less CD14-dependent and could proceed in the absence of serum as an LBP source. On the other hand, the involvement of CD14 was crucial for the binding of 1000 ng/mL of sLPS judging from an inhibitory effect of the anti-CD14 antibody. The binding of sLPS was also strongly inhibited by dextran sulfate, a competitive ligand of scavenger receptors (SR). In the presence of dextran sulfate, sLPS-induced production of TNF-α was upregulated about 1.6-fold. The data indicate that CD14 together with SR participates in the binding of high doses of sLPS. However, CD14 contribution to TNF α production induced by high concentrations of sLPS and rLPS can be limited.
Indexed as
Identifiers
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.