Evidence map›Paper›PMID 34349763›Full record

ArticleFrontiers in immunology2021

A Synthetic Peptide Designed to Neutralize Lipopolysaccharides Attenuates Metaflammation and Diet-Induced Metabolic Derangements in Mice.

Shireen Mohammad, Sura Al Zoubi, Debora Collotta, Nadine Krieg, Bianka Wissuwa, Gustavo Ferreira Alves, Gareth S D Purvis, Giuseppe Danilo Norata, Andrea Baragetti, Alberico Luigi Catapano and 10 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Frontiers in nutrition · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 10 institutions in 4 countries.

Shireen MohammadWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Sura Al ZoubiWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Debora CollottaDepartment of Drug Science and Technology, University of Turin, Turin, Italy.
Nadine KriegDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Bianka WissuwaDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Gustavo Ferreira AlvesDepartment of Drug Science and Technology, University of Turin, Turin, Italy.
Gareth S D PurvisWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Giuseppe Danilo NorataDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.
Andrea BaragettiDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.
Alberico Luigi CatapanoDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.
Egle SolitoWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Elisabeth ZechendorfDepartment of Intensive Care and Intermediate Care, University Hospital RWTH Aachen, Aachen, Germany.
Tobias SchürholzDepartment of Intensive Care and Intermediate Care, University Hospital RWTH Aachen, Aachen, Germany.
Wilmar Correa-VargasForschungszentrum Borstel, Department of Biophysics, Borstel, Germany.
Klaus BrandenburgBrandenburg Antiinfektiva GmbH, c/o Forschungszentrum Borstel, Borstel, Germany.
Sina M ColdeweyDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.
Massimo CollinoDepartment of Neurosciences "Rita Levi Montalcini", University of Turin, Turin, Italy.
Muhammad M YaqoobWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Lukas MartinWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Christoph ThiemermannWilliam Harvey Research Institute, Bart's and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.
Jena University Hospital · DERWTH Aachen University · DEUniversity of Turin · ITWilliam Harvey Research Institute · GBMultiMedica · ITAl-Balqa Applied University · JOQueen Mary University of London · GBResearch Center Borstel - Leibniz Lung Center · DEUniversity of Milan · ITUniversity of Oxford · GB

Funding

British Heart Foundation FS/17/69/33484
6 · The paper itself

Abstract

Metabolic endotoxemia has been suggested to play a role in the pathophysiology of metaflammation, insulin-resistance and ultimately type-2 diabetes mellitus (T2DM). The role of endogenous antimicrobial peptides (AMPs), such as the cathelicidin LL-37, in T2DM is unknown. We report here for the first time that patients with T2DM compared to healthy volunteers have elevated plasma levels of LL-37. In a reverse-translational approach, we have investigated the effects of the AMP, peptide 19-2.5, in a murine model of high-fat diet (HFD)-induced insulin-resistance, steatohepatitis and T2DM. HFD-fed mice for 12 weeks caused obesity, an impairment in glycemic regulations, hypercholesterolemia, microalbuminuria and steatohepatitis, all of which were attenuated by Peptide 19-2.5. The liver steatosis caused by feeding mice a HFD resulted in the activation of nuclear factor kappa light chain enhancer of activated B cells (NF-ĸB) (phosphorylation of inhibitor of kappa beta kinase (IKK)α/β, IκBα, translocation of p65 to the nucleus), expression of NF-ĸB-dependent protein inducible nitric oxide synthase (iNOS) and activation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome, all of which were reduced by Peptide 19-2.5. Feeding mice, a HFD also resulted in an enhanced expression of the lipid scavenger receptor cluster of differentiation 36 (CD36) secondary to activation of extracellular signal-regulated kinases (ERK)1/2, both of which were abolished by Peptide 19-2.5. Taken together, these results demonstrate that the AMP, Peptide 19-2.5 reduces insulin-resistance, steatohepatitis and proteinuria. These effects are, at least in part, due to prevention of the expression of CD36 and may provide further evidence for a role of metabolic endotoxemia in the pathogenesis of metaflammation and ultimately T2DM. The observed increase in the levels of the endogenous AMP LL-37 in patients with T2DM may serve to limit the severity of the disease.

Indexed as

InflammationAnimalsAntimicrobial Cationic PeptidesAntimicrobial PeptidesCathelicidinsDiabetes Mellitus, Type 2Diet, High-FatEndotoxemiaHumansLipopolysaccharidesMaleMiceMice, Inbred C57BLAntimicrobial Cationic PeptidesAntimicrobial PeptidesCathelicidinsLipopolysaccharidesantimicrobial peptidehigh-fat dietinsulin resistancemicroalbuminuriapeptide 19-2.5steatohepatitistype-2 diabetes

Identifiers

PMID34349763
PMCPMC8328475
OpenAlexW3185178753

What OpenQuestion holds

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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.