Evidence map›Paper›PMID 34131160›Full record

ArticleScientific reports2021

Plantaricin NC8 αβ prevents Staphylococcus aureus-mediated cytotoxicity and inflammatory responses of human keratinocytes.

Amani Musa, Emanuel Wiman, Robert Selegård, Daniel Aili, Torbjörn Bengtsson, Hazem Khalaf

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Antibacterial Effects of Synthetic Plantaricins AgainstAntibiotics (Basel, Switzerland) · 2025
    Article
  2. Inhibition ofmSphere · 2024
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Preventing microbe colonization on avocado (Frontiers in microbiology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. 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

6 authors at 2 institutions in 1 country.

Amani MusaSchool of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 42A, 703 62, Örebro, Sweden. amani.musa@oru.se.
Emanuel WimanSchool of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 42A, 703 62, Örebro, Sweden. emanuel.wiman@oru.se.
Robert SelegårdLaboratory of Molecular Materials, Division of Biophysics and Bioengineering, Department of Physics, Chemistry and Biology (IFM), Linköping University, Linköping, Sweden.
Daniel AiliLaboratory of Molecular Materials, Division of Biophysics and Bioengineering, Department of Physics, Chemistry and Biology (IFM), Linköping University, Linköping, Sweden.
Torbjörn BengtssonSchool of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 42A, 703 62, Örebro, Sweden.
Hazem KhalafSchool of Medical Sciences, Örebro University, Campus USÖ, Södra Grev Rosengatan 42A, 703 62, Örebro, Sweden.
Örebro University · SELinköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug resistance bacteria constitue an increasing global health problem and the development of novel therapeutic strategies to face this challenge is urgent. Antimicrobial peptides have been proven as potent agents against pathogenic bacteria shown by promising in vitro results. The aim of this study was to characterize the antimicrobial effects of PLNC8 αβ on cell signaling pathways and inflammatory responses of human keratinocytes infected with S. aureus. PLNC8 αβ did not affect the viability of human keratinocytes but upregulated several cytokines (IL-1β, IL-6, CXCL8), MMPs (MMP1, MMP2, MMP9, MMP10) and growth factors (VEGF and PDGF-AA), which are essential in cell regeneration. S. aureus induced the expression of several inflammatory mediators at the gene and protein level and PLNC8 αβ was able to significantly suppress these effects. Intracellular signaling events involved primarily c-Jun via JNK, c-Fos and NFκB, suggesting their essential role in the initiation of inflammatory responses in human keratinocytes. PLNC8 αβ was shown to modulate early keratinocyte responses, without affecting their viability. The peptides have high selectivity towards S. aureus and were efficient at eliminating the bacteria and counteracting their inflammatory and cytotoxic effects, alone and in combination with low concentrations of gentamicin. We propose that PLNC8 αβ may be developed to combat infections caused by Staphylococcus spp.

Indexed as

Anti-Bacterial AgentsCell LineCell SurvivalCytokinesGene Expression RegulationHumansIntercellular Signaling Peptides and ProteinsInterleukin-1betaKeratinocytesStaphylococcal InfectionsStaphylococcus aureusTranscriptional ActivationAnti-Bacterial AgentsCytokinesIL1B protein, humanIntercellular Signaling Peptides and ProteinsInterleukin-1beta

Identifiers

PMID34131160
PMCPMC8206081
OpenAlexW3171984567

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.