Evidence map›Paper›PMID 30669987›Full record

ArticleBMC genomics2019

Transcriptionally induced enhancers in the macrophage immune response to Mycobacterium tuberculosis infection.

Elena Denisenko, Reto Guler, Musa Mhlanga, Harukazu Suzuki, Frank Brombacher, Sebastian Schmeier

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
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  4. AProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Cellular and Molecular Network Characteristics ofInternational journal of molecular sciences · 2024
    Article
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  9. Korean circulation journal · 2021
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  16. A Comparative Analysis ofInternational journal of molecular sciences · 2019
    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 4 institutions in 4 countries.

Elena DenisenkoMassey University, Institute of Natural and Mathematical Sciences, Albany, Auckland, New Zealand.
Reto GulerDivision of Immunology and South African Medical Research Council (SAMRC) Immunology of Infectious Diseases, Faculty of Health Sciences, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town, South Africa.
Musa MhlangaGene Expression and Biophysics Group, CSIR Synthetic Biology ERA, Pretoria, South Africa.
Harukazu SuzukiDivision of Genomic Technologies, RIKEN Center for Integrative Medical Sciences, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Japan.
Frank BrombacherDivision of Immunology and South African Medical Research Council (SAMRC) Immunology of Infectious Diseases, Faculty of Health Sciences, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town, South Africa.
Sebastian SchmeierMassey University, Institute of Natural and Mathematical Sciences, Albany, Auckland, New Zealand. s.schmeier@massey.ac.nz.ORCID http://orcid.org/0000-0002-3947-8226
Massey University · NZSouth African Medical Research Council · ZARIKEN Center for Integrative Medical Sciences · JPUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTuberculosis is a life-threatening infectious disease caused by Mycobacterium tuberculosis (M.tb). M.tb subverts host immune responses to build a favourable niche and survive inside of host macrophages. Macrophages can control or eliminate the infection, if acquire appropriate functional phenotypes. Transcriptional regulation is a key process that governs the activation and maintenance of these phenotypes. Among the factors orchestrating transcriptional regulation during M.tb infection, transcriptional enhancers still remain unexplored.

resultsWe analysed transcribed enhancers in M.tb-infected mouse bone marrow-derived macrophages. We established a link between known M.tb-responsive transcription factors and transcriptional activation of enhancers and their target genes. Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4. We report enhancers acquiring transcription de novo upon infection. Finally, we link highly transcriptionally induced enhancers to activation of genes with previously unappreciated roles in M.tb infection, such as Fbxl3, Tapt1, Edn1, and Hivep1.

conclusionsOur findings suggest the importance of macrophage host transcriptional enhancers during M.tb infection. Our study extends current knowledge of the regulation of macrophage responses to M.tb infection and provides a basis for future functional studies on enhancer-gene interactions in this process.

Indexed as

Enhancer Elements, GeneticGene Expression RegulationAnimalsBinding SitesMacrophagesMice, Inbred BALB CMycobacterium tuberculosisTranscription FactorsTranscription, GeneticTranscription FactorseRNAMacrophagesTranscriptional enhancersTranscriptional regulationTuberculosis

Identifiers

PMID30669987
PMCPMC6341744
OpenAlexW2916238870

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.