Evidence map›Paper›PMID 17283090›Full record

ArticleInfection and immunity2007

A caspase-independent pathway mediates macrophage cell death in response to Mycobacterium tuberculosis infection.

Mary P O'Sullivan, Seonadh O'Leary, Deirdre M Kelly, Joseph Keane

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 74 citations in OpenAlex.

  1. Isotopic tracing inVirulence · 2026
    Article
  2. Review
  3. Article
  4. Review
  5. Lactate Metabolism and Signaling in Tuberculosis and Cancer: A Comparative Review.Frontiers in cellular and infection microbiology · 2021
    Review
  6. Article
  7. Review
  8. Frontiers in cellular and infection microbiology · 2020
    Article
  9. TLR-2 mediated cytosolic-CaScientific reports · 2019
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Heparin-binding Hemagglutinin ofFrontiers in cellular and infection microbiology · 2017
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Cell death paradigms in the pathogenesis of Mycobacterium tuberculosis infection.Frontiers in cellular and infection microbiology · 2014
    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

4 authors at 1 institution in 1 country.

Mary P O'SullivanDepartmrent of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin and St. James's Hospital, CResT, Dublin 8, Ireland.
Seonadh O'Leary
Deirdre M Kelly
Joseph Keane
Trinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages can undergo apoptosis after infection with Mycobacterium tuberculosis. This macrophage response deprives the bacillus of its niche cell and supports the host response through better antigen presentation. The intracellular pathways of apoptosis that elaborate this macrophage response are not well understood. To address this issue, we investigated the contribution of various apoptosis pathways to M. tuberculosis-induced macrophage cell death. We found that macrophages die in a caspase-independent manner after infection with M. tuberculosis (at multiplicities of infection ranging from 1 to 20). There was evidence for the involvement of both the mitochondria (cleavage of Bid) and the lysosomes (cathepsin-mediated DNA fragmentation) in this cell death pathway. Dying macrophages displayed several features typical of apoptosis, including DNA fragmentation, nuclear condensation, and exposure of phosphatidylserine on the plasma membrane. However, nuclear fragmentation was not observed, which suggests that M. tuberculosis-induced cell death differs in some respects from classical apoptosis. This novel mechanism of cell death was blocked by serine protease inhibitors. A better understanding of this protective macrophage response may direct new vaccine and treatment options.

Indexed as

ApoptosisBacillusBH3 Interacting Domain Death Agonist ProteinCaspasesCathepsinsCell LineCells, CulturedCell SurvivalDNA FragmentationHumansLysosomesMacrophagesMitochondriaMycobacterium tuberculosisPhosphatidylserinesSerine Proteinase Inhibitors4-(2-aminoethyl)benzenesulfonylfluorideBH3 Interacting Domain Death Agonist ProteinBID protein, humanCaspasesCathepsinsPhosphatidylserinesSerine Proteinase InhibitorsSulfones

Identifiers

PMID17283090
PMCPMC1865710
OpenAlexW2111397679

What OpenQuestion holds

Textmetadata
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.