Evidence map›Paper›PMID 25658322›Full record

ArticlePLoS pathogens2015

Cytosolic access of Mycobacterium tuberculosis: critical impact of phagosomal acidification control and demonstration of occurrence in vivo.

Roxane Simeone, Fadel Sayes, Okryul Song, Matthias I Gröschel, Priscille Brodin, Roland Brosch, Laleh Majlessi

Abstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed
–field-weighted citation impact
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

114 citing papers in PubMed.

  1. HowVaccines · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. ACOD1-mediated lysosomal membrane permeabilization contributes toProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Comparative transcriptomic signatures of virulent and attenuatedFrontiers in cellular and infection microbiology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Frontiers in tuberculosis · 2024
    Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023
    Review
  17. Article
  18. Review
  19. Article
  20. Article

54 more citing papers are in PubMed but not listed here.

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.

Roxane SimeoneInstitut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France; Inserm U1019, CNRS UMR8204, Université de Lille-Nord de France, Institut Pasteur de Lille, Center for Infection and Immunity, Lille, France.
Fadel SayesInstitut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France.
Okryul SongInserm U1019, CNRS UMR8204, Université de Lille-Nord de France, Institut Pasteur de Lille, Center for Infection and Immunity, Lille, France.
Matthias I GröschelInstitut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France.
Priscille BrodinInserm U1019, CNRS UMR8204, Université de Lille-Nord de France, Institut Pasteur de Lille, Center for Infection and Immunity, Lille, France.
Roland BroschInstitut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France.
Laleh MajlessiInstitut Pasteur, Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mtb) uses efficient strategies to evade the eradication by professional phagocytes, involving--as recently confirmed--escape from phagosomal confinement. While Mtb determinants, such as the ESX-1 type VII secretion system, that contribute to this phenomenon are known, the host cell factors governing this important biological process are yet unexplored. Using a newly developed flow-cytometric approach for Mtb, we show that macrophages expressing the phagosomal bivalent cation transporter Nramp-1, are much less susceptible to phagosomal rupture. Together with results from the use of the phagosome acidification inhibitor bafilomycin, we demonstrate that restriction of phagosomal acidification is a prerequisite for mycobacterial phagosomal rupture and cytosolic contact. Using different in vivo approaches including an enrichment and screen for tracking rare infected phagocytes carrying the CD45.1 hematopoietic allelic marker, we here provide first and unique evidence of M. tuberculosis-mediated phagosomal rupture in mouse spleen and lungs and in numerous phagocyte types. Our results, linking the ability of restriction of phagosome acidification to cytosolic access, provide an important conceptual advance for our knowledge on host processes targeted by Mtb evasion strategies.

Indexed as

AnimalsBacterial Secretion SystemsCation Transport ProteinsCell Line, TumorHumansHydrogen-Ion ConcentrationLeukocyte Common AntigensMacrophagesMiceMice, Mutant StrainsMycobacterium tuberculosisNatural Resistance-associated Macrophage Protein 1PhagosomesTuberculosisBacterial Secretion SystemsCation Transport ProteinsLeukocyte Common AntigensNatural Resistance-associated Macrophage Protein 1PTPRC protein, humanPtprc protein, mouse

Identifiers

PMID25658322
PMCPMC4450080

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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.