Evidence map›Paper›PMID 37737955›Full record

ArticleThe Journal of cell biology2023

Peroxisomal ROS control cytosolic Mycobacterium tuberculosis replication in human macrophages.

Enrica Pellegrino, Beren Aylan, Claudio Bussi, Antony Fearns, Elliott M Bernard, Natalia Athanasiadi, Pierre Santucci, Laure Botella, Maximiliano G Gutierrez

Open access · hybridAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. The peroxisome: an update on mysteries 3.0.Histochemistry and cell biology · 2024
    Review
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

9 authors at 1 institution in 1 country.

Enrica PellegrinoHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-3918-2310
Beren AylanHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0009-0008-7741-2712
Claudio BussiHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-9396-9042
Antony FearnsHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0001-9937-8545
Elliott M BernardHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-2761-3790
Natalia AthanasiadiHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0009-0006-4453-0611
Pierre SantucciHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0002-6291-3425
Laure BotellaHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-2776-4118
Maximiliano G GutierrezHost-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.ORCID 0000-0003-3199-0337
The Francis Crick Institute · GB

Funding

Cancer Research UK FC001092Medical Research Council FC001092Wellcome Trust FC001092
6 · The paper itself

Abstract

Peroxisomes are organelles involved in many metabolic processes including lipid metabolism, reactive oxygen species (ROS) turnover, and antimicrobial immune responses. However, the cellular mechanisms by which peroxisomes contribute to bacterial elimination in macrophages remain elusive. Here, we investigated peroxisome function in iPSC-derived human macrophages (iPSDM) during infection with Mycobacterium tuberculosis (Mtb). We discovered that Mtb-triggered peroxisome biogenesis requires the ESX-1 type 7 secretion system, critical for cytosolic access. iPSDM lacking peroxisomes were permissive to Mtb wild-type (WT) replication but were able to restrict an Mtb mutant missing functional ESX-1, suggesting a role for peroxisomes in the control of cytosolic but not phagosomal Mtb. Using genetically encoded localization-dependent ROS probes, we found peroxisomes increased ROS levels during Mtb WT infection. Thus, human macrophages respond to the infection by increasing peroxisomes that generate ROS primarily to restrict cytosolic Mtb. Our data uncover a peroxisome-controlled, ROS-mediated mechanism that contributes to the restriction of cytosolic bacteria.

Indexed as

MacrophagesMycobacterium tuberculosisPeroxisomesReactive Oxygen SpeciesCytosolHumansType VII Secretion SystemsReactive Oxygen SpeciesType VII Secretion Systems

Identifiers

PMID37737955
PMCPMC10515436
OpenAlexW4386945033

What Socratic 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 Socratic graph.