Evidence map›Paper›PMID 37630200›Full record

ArticleMolecules (Basel, Switzerland)2023

Exploring Species-Specificity in TLR4/MD-2 Inhibition with Amphiphilic Lipid A Mimicking Glycolipids.

Alessio Borio, Aurora Holgado, Christina Passegger, Herbert Strobl, Rudi Beyaert, Holger Heine, Alla Zamyatina

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 27% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Salvimulticanol from3 Biotech · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Alessio BorioInstitute of Organic Chemistry, Department of Chemistry, University of Natural Resources and Life Sciences, Muthgasse 18, 1190 Vienna, Austria.ORCID 0000-0002-8905-7569
Aurora HolgadoUnit of Molecular Signal Transduction in Inflammation, VIB-UGent Center for Inflammation Research, Department for Biomedical Molecular Biology, Ghent University, Technologiepark 71, B-9052 Ghent, Belgium.
Christina PasseggerDivision of Immunology and Pathophysiology, Medical University Graz, Heinrichstraße 31, 8010 Graz, Austria.
Herbert StroblDivision of Immunology and Pathophysiology, Medical University Graz, Heinrichstraße 31, 8010 Graz, Austria.
Rudi BeyaertUnit of Molecular Signal Transduction in Inflammation, VIB-UGent Center for Inflammation Research, Department for Biomedical Molecular Biology, Ghent University, Technologiepark 71, B-9052 Ghent, Belgium.ORCID 0000-0002-5704-582X
Holger HeineResearch Group Innate Immunity, Priority Area Chronic Lung Diseases, Research Center Borstel, Leibniz Lung Center, Airway Research Center North (ARCN), German Center for Lung Research (DZL), Parkallee 22, 23845 Borstel, Germany.ORCID 0000-0001-8128-5068
Alla ZamyatinaInstitute of Organic Chemistry, Department of Chemistry, University of Natural Resources and Life Sciences, Muthgasse 18, 1190 Vienna, Austria.ORCID 0000-0002-4001-3522
BOKU University · ATMedical University of Graz · ATVIB-UGent Center for Inflammation Research · BEResearch Center Borstel - Leibniz Lung Center · DE

Funding

Austrian Science Fund FWF P 32397
6 · The paper itself

Abstract

The Toll-like receptor 4 (TLR4)/myeloid differentiation factor 2 (MD-2) complex is a key receptor of the innate immune system and a major driver of inflammation that is responsible for the multifaceted defense response to Gram-negative infections. However, dysfunction in the tightly regulated mechanisms of TLR4-mediated signaling leads to the uncontrolled upregulation of local and systemic inflammation, often resulting in acute or chronic disease. Therefore, the TLR4/MD-2 receptor complex is an attractive target for the design and development of anti-inflammatory therapies which aim to control the unrestrained activation of TLR4-mediated signaling. Complex structure-activity relationships and species-specificity behind ligand recognition by the TLR4/MD-2 complex complicate the development of MD-2-specific TLR4 antagonists. The restriction of the conformational flexibility of the disaccharide polar head group is one of the key structural features of the newly developed lipid A-mimicking glycophospholipids, which are potential inhibitors of TLR4-mediated inflammation. Since phosphorylation has a crucial influence on MD-2-ligand interaction, glycolipids with variable numbers and positioning of phosphate groups were synthesized and evaluated for their ability to inhibit TLR4-mediated pro-inflammatory signaling in human and murine immune cells. A bis-phosphorylated glycolipid was found to have nanomolar antagonist activity on human TLR4 while acting as a partial agonist on murine TLR4. The glycolipid inhibited mTLR4/MD-2-mediated cytokine release, acting as an antagonist in the presence of lipopolysaccharide (LPS), but at the same time induced low-level cytokine production.

Indexed as

Lipid AToll-Like Receptor 4AnimalsCell DifferentiationCytokinesGlycolipidsHumansInflammationLigandsMiceCytokinesGlycolipidsLigandsLipid ATLR4 protein, humanToll-Like Receptor 4carbohydrate-based inhibitorscarbohydratesinflammationlipopolysaccharideToll-like receptor

Identifiers

PMID37630200
PMCPMC10459247
OpenAlexW4385665317

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.