Evidence map›Paper›PMID 28445535›Full record

ArticlePloS one2017

microRNA-125a-3p is regulated by MyD88 in Legionella pneumophila infection and targets NTAN1.

Elisa Jentho, Malena Bodden, Christine Schulz, Anna-Lena Jung, Kerstin Seidel, Bernd Schmeck, Wilhelm Bertrams

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Graft-Host Interaction and Its Effect on Wound Repair Using Mouse Models.International journal of molecular sciences · 2023
    Article
  4. Review
  5. Regulation of Toll-like receptor-mediated inflammatory response by microRNA-152-3p-mediated demethylation of MyD88 in systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  6. Article
  7. Review
  8. 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 2 institutions in 1 country.

Elisa JenthoInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
Malena BoddenInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
Christine SchulzInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
Anna-Lena JungInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
Kerstin SeidelInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
Bernd SchmeckInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.ORCID http://orcid.org/0000-0002-2767-3606
Wilhelm BertramsInstitute for Lung Research/iLung, German Center for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, Marburg, Germany.
German Center for Lung Research · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLegionella pneumophila (L. pneumophila) is a causative agent of severe pneumonia. It is highly adapted to intracellular replication and manipulates host cell functions like vesicle trafficking and mRNA translation to its own advantage. However, it is still unknown to what extent microRNAs (miRNAs) are involved in the Legionella-host cell interaction.

methodsWT and MyD88-/- murine bone marrow-derived macrophages (BMM) were infected with L. pneumophila, the transcriptome was analyzed by high throughput qPCR array (microRNAs) and conventional qPCR (mRNAs), and mRNA-miRNA interaction was validated by luciferase assays with 3´-UTR mutations and western blot.

resultsL. pneumophila infection caused a pro-inflammatory reaction and significant miRNA changes in murine macrophages. In MyD88-/- cells, induction of inflammatory markers, such as Ccxl1/Kc, Il6 and miR-146a-5p was reduced. Induction of miR-125a-3p was completely abrogated in MyD88-/- cells. Target prediction analyses revealed N-terminal asparagine amidase 1 (NTAN1), a factor from the n-end rule pathway, to be a putative target of miR-125a-3p. This interaction could be confirmed by luciferase assay and western blot.

conclusionTaken together, we characterized the miRNA regulation in L. pneumophila infection with regard to MyD88 signaling and identified NTAN1 as a target of miR-125a-3p. This finding unravels a yet unknown feature of Legionella-host cell interaction, potentially relevant for new treatment options.

Indexed as

3' Untranslated RegionsAmidohydrolasesAnimalsBase SequenceChemokine CXCL1GenotypeInterleukin-6Legionella pneumophilaLegionnaires' DiseaseMacrophagesMiceMice, KnockoutMicroRNAsMyeloid Differentiation Factor 88RAW 264.7 CellsSequence Alignment3' Untranslated RegionsAmidohydrolasesChemokine CXCL1Interleukin-6MicroRNAsMyd88 protein, mouseMyeloid Differentiation Factor 88N-terminal asparagine amidohydrolase

Identifiers

PMID28445535
PMCPMC5406027
OpenAlexW2609497793

What OpenQuestion holds

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Registered trials

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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.