Evidence map›Paper›PMID 22802345›Full record

ArticleInfection and immunity2012

A ferritin mutant of Mycobacterium tuberculosis is highly susceptible to killing by antibiotics and is unable to establish a chronic infection in mice.

Ruchi Pandey, G Marcela Rodriguez

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Meta-analysis reveals a core iron-responsive gene signature in Mycobacterium tuberculosis linking siderophore biosynthesis, virulence, and metabolic adaptation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Pooled it
  2. Article
  3. Metabolic perturbation reduces antibiotic tolerance inMicrobiology (Reading, England) · 2026
    Article
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  15. Article
  16. Review
  17. Biomedicines · 2022
    Article
  18. The Iron Response ofFrontiers in cellular and infection microbiology · 2022
    Review
  19. Review
  20. Cryo-EM structure ofProceedings of the National Academy of Sciences of the United States of America · 2021
    Article

4 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

2 authors at 1 institution.

Ruchi PandeyPublic Health Research Institute and Department of Medicine, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, New Jersey, USA.
G Marcela Rodriguez
Rutgers New Jersey Medical School

Funding

M TUBERCULOSIS SURVIVAL AND GROWTH IN VIVOR01AI044856 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RODRIGUEZ, GLORIA MARCELA, SMITH, ISSAR · 1999 to 2014
$6.8M
Mechanisms and regulation of Mycobacterium tuberculosis iron acquisitionR56AI044856 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RODRIGUEZ, GLORIA MARCELA, SMITH, ISSAR · 2009 to 2009
$585k
NIAID NIH HHS AI044856NIAID NIH HHS R01 AI044856NIAID NIH HHS R56 AI044856
6 · The paper itself

Abstract

Iron is an essential, elusive, and potentially toxic nutrient for most pathogens, including Mycobacterium tuberculosis. Due to the poor solubility of ferric iron under aerobic conditions, free iron is not found in the host. M. tuberculosis requires specialized iron acquisition systems to replicate and cause disease. It also depends on a strict control of iron metabolism and intracellular iron levels to prevent iron-mediated toxicity. Under conditions of iron sufficiency, M. tuberculosis represses iron acquisition and induces iron storage, suggesting an important role for iron storage proteins in iron homeostasis. M. tuberculosis synthesizes two iron storage proteins, a ferritin (BfrB) and a bacterioferritin (BfrA). The individual contributions of these proteins to the adaptive response of M. tuberculosis to changes in iron availability are not clear. By generating individual knockout strains of bfrA and bfrB, the contribution of each one of these proteins to the maintenance of iron homeostasis was determined. The effect of altered iron homeostasis, resulting from impaired iron storage, on the resistance of M. tuberculosis to in vitro and in vivo stresses was examined. The results show that ferritin is required to maintain iron homeostasis, whereas bacterioferritin seems to be dispensable for this function. M. tuberculosis lacking ferritin suffers from iron-mediated toxicity, is unable to persist in mice, and, most importantly, is highly susceptible to killing by antibiotics, showing that endogenous oxidative stress can enhance the antibiotic killing of this important pathogen. These results are relevant for the design of new therapeutic strategies against M. tuberculosis.

Indexed as

Adaptation, PhysiologicalAnimalsAntitubercular AgentsChronic DiseaseFemaleFerritinsGene DeletionGene Expression Regulation, BacterialHomeostasisIronLungMiceMice, Inbred C57BLMicrobial Sensitivity TestsMycobacterium tuberculosisOxidative StressAntitubercular AgentsFerritinsIron

Identifiers

PMID22802345
PMCPMC3457556
OpenAlexW2125777345

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.