Evidence map›Paper›PMID 22960076›Full record

ArticleThe American journal of pathology2012

Spontaneous latency in a rabbit model of pulmonary tuberculosis.

Selvakumar Subbian, Liana Tsenova, Paul O'Brien, Guibin Yang, Nicole L Kushner, Sven Parsons, Blas Peixoto, Dorothy Fallows, Gilla Kaplan

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Model systems to studyFrontiers in cellular and infection microbiology · 2025
    Review
  6. Methods and Models for StudyingInternational journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Mathematical modeling suggests heterogeneous replication ofbioRxiv : the preprint server for biology · 2024
    Article
  11. Immunopathology of PulmonaryInternational journal of molecular sciences · 2024
    Article
  12. Review
  13. Review
  14. Animal models for COVID-19 and tuberculosis.Frontiers in immunology · 2023
    Review
  15. Microorganisms · 2022
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

9 authors at 3 institutions in 2 countries.

Selvakumar SubbianLaboratory of Mycobacterial Immunity and Pathogenesis, The Public Health Research Institute Center at the University of Medicine and Dentistry of New Jersey, Newark, USA.
Liana Tsenova
Paul O'Brien
Guibin Yang
Nicole L Kushner
Sven Parsons
Blas Peixoto
Dorothy Fallows
Gilla Kaplan
New Jersey Institute of Technology · USUniversity Hospital, Newark · USStellenbosch University · ZA

Funding

Host &Pathogen Determinants of M tuberculosis LatencyR01AI054338 · NIAID · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI KAPLAN, GILLA · 2002 to 2011
$5.0M
NIAID NIH HHS R01 AI054338PHS HHS R01 54338
6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mtb), the causative agent of tuberculosis (TB), is an exquisitely adapted human pathogen capable of surviving for decades in the lungs of immune-competent individuals in the absence of disease. The World Health Organization estimates that 2 billion people have latent TB infection (LTBI), defined by a positive immunological response to Mtb antigens, with no clinical signs of disease. A better understanding of host and pathogen determinants of LTBI and subsequent reactivation would benefit TB control efforts. Animal models of LTBI have been hampered generally by an inability to achieve complete bacillary clearance. Herein, we have characterized a rabbit model of LTBI in which, similar to most humans, complete clearance of pulmonary Mtb infection and pathological characteristics occurs spontaneously. The evidence that Mtb-CDC1551-infected rabbits achieve LTBI, rather than sterilization, is based on the ability of the bacilli to be reactivated after immune suppression. These rabbits showed early activation of T cells and macrophages and an early peak in the TNFα level, which decreased in association with clearance of bacilli from the lungs. In the absence of sustained tumor necrosis factor-α production, no necrosis was seen in the evolving lung granulomas. In addition, bacillary control was associated with down-regulation of several metalloprotease genes and an absence of lung fibrosis. This model will be used to characterize molecular markers of protective immunity and reactivation.

Indexed as

AnimalsBacterial LoadCell ProliferationDisease Models, AnimalFemaleFlow CytometryGene Expression ProfilingHumansLatent TuberculosisLungLymphocyte ActivationMacrophage ActivationMycobacterium tuberculosisPulmonary FibrosisRabbitsSignal Transduction

Identifiers

PMID22960076
PMCPMC3483799
OpenAlexW2065100101

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.