ArticleInnate immunity2015
Monophosphoryl lipid A inhibits the cytokine response of endothelial cells challenged with LPS.
Article in Innate immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 17 citations in OpenAlex.
- Phosphorylation shapes antigen presentation and immune recognition: mechanistic insights and translational perspectives.Frontiers in immunology · 2026Review
- Dectin-1 stimulating β-glucans inhibit Chlamydia infections both in vitro and in vivo.Pathogens and disease · 2025Article
- APR-246 increases tumor antigenicity independent of p53.Life science alliance · 2024Article
- Developing a multiepitope vaccine for the prevention of SARS-CoV-2 and monkeypox virus co-infection: A reverse vaccinology analysis.International immunopharmacology · 2023Article
- Cell penetrating peptides coupled to an endothelial nitric oxide synthase sequence alter endothelial permeability.Tissue barriers · 2022Article
- Trained Immunity and Reactivity of Macrophages and Endothelial Cells.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- TLR-4 Signaling vs. Immune Checkpoints, miRNAs Molecules, Cancer Stem Cells, and Wingless-Signaling Interplay in Glioblastoma Multiforme-Future Perspectives.International journal of molecular sciences · 2020Review
- BMP-9 Modulates the Hepatic Responses to LPS.Cells · 2020Article
- Monophosphoryl Lipid a Attenuates Multiorgan Dysfunction During Post-Burn Pseudomonas Aeruginosa Pneumonia in Sheep.Shock (Augusta, Ga.) · 2020Article
- In situ vaccination with defined factors overcomes T cell exhaustion in distant tumors.The Journal of clinical investigation · 2019Article
- Endothelial nitric oxide synthase modulates Toll-like receptor 4-mediated IL-6 production and permeability via nitric oxide-independent signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Potentiation and tolerance of toll-like receptor priming in human endothelial cells.Translational research : the journal of laboratory and clinical medicine · 2017Article
- Endothelial cell tolerance to lipopolysaccharide challenge is induced by monophosphoryl lipid A.Clinical science (London, England : 1979) · 2016Article
- Association of O-Antigen Serotype with the Magnitude of Initial Systemic Cytokine Responses and Persistence in the Urinary Tract.Journal of bacteriology · 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 1 institution in 1 country.
Funding
Abstract
Monophosphoryl lipid A (MPLA) is a TLR4 agonist that is used as an immunomodulator in human vaccines; additionally, it has been shown to be protective in models of sepsis. As endothelial cells regulate inflammation, we hypothesized that MPLA would decrease activation of human umbilical vein endothelial cells (HUVECs) to LPS. We studied HUVECs challenged with LPS (100 ng/ml), MPLA (0.001-100 µg/ml) or a combination. Secretion of IL-6, RANTES (CCL5) and IP-10 (CXCL10) were assessed by ELISA. Activation of MAPK phosphorylation and cytokine transcription were assessed by Western blot analysis and PCR, respectively. MPLA alone was a weak stimulator of myeloid differentiation primary response protein 88-dependent IL-6 and did not induce TIR-domain-containing adapter-inducing IFN-β (TRIF)-dependent chemokine responses. MPLA significantly reduced LPS-mediated IL-6 production. This inhibitory effect was also conferred for the TRIF-dependent chemokines RANTES and IP-10. Inhibition of LPS-mediated activation by MPLA was associated with reduced p38 phosphorylation and mRNAs encoding inflammatory cytokines. MPLA inhibition of LPS signaling appeared to be at the level of the TLR4 receptor, acting as a receptor antagonist with weak agonistic properties. This study provides evidence of a novel mechanism for the inhibitory effect of MPLA on LPS-induced endothelial activation.
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.