Evidence map›Paper›PMID 22737072›Full record

ArticlePLoS pathogens2012

Linking the transcriptional profiles and the physiological states of Mycobacterium tuberculosis during an extended intracellular infection.

Kyle H Rohde, Diogo F T Veiga, Shannon Caldwell, Gábor Balázsi, David G Russell

Abstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 1 pooled it
–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

161 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. mBio · 2026
    Article
  5. Review
  6. bioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Frontiers in cellular and infection microbiology · 2025
    Article
  11. ACS chemical biology · 2024
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. TargetingMicrobiology (Reading, England) · 2024
    Review
  18. Article
  19. Article
  20. Frontiers in cellular and infection microbiology · 2023
    Article

101 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

5 authors.

Kyle H RohdeDepartment of Microbiology and Immunology, Cornell University, Ithaca, New York, United States of America. Kyle.Rohde@ucf.edu
Diogo F T Veiga
Shannon Caldwell
Gábor Balázsi
David G Russell

Funding

Environmental Cues and Responses in TuberculosisR01AI067027 · NIAID · CORNELL UNIVERSITY · PI RUSSELL, DAVID G · 2006 to 2015
$4.0M
Mapping and modeling host-pathogen interactions in TB latency and reactivationR01HL106788 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI BALAZSI, GABOR, GENNARO, MARIA LAURA · 2010 to 2013
$3.1M
Connecting the selection of noisy gene expression deviants to genetic evolutionDP2OD006481 · OD · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BALAZSI, GABOR · 2009 to 2009
$2.3M
NHLBI NIH HHS 1-R01-HL106788NHLBI NIH HHS R01 HL106788NIAID NIH HHS AI067027NIAID NIH HHS R01 AI067027NIH HHS 1DP2 OD006481-01NIH HHS DP2 OD006481
6 · The paper itself

Abstract

Intracellular pathogens such as Mycobacterium tuberculosis have evolved strategies for coping with the pressures encountered inside host cells. The ability to coordinate global gene expression in response to environmental and internal cues is one key to their success. Prolonged survival and replication within macrophages, a key virulence trait of M. tuberculosis, requires dynamic adaptation to diverse and changing conditions within its phagosomal niche. However, the physiological adaptations during the different phases of this infection process remain poorly understood. To address this knowledge gap, we have developed a multi-tiered approach to define the temporal patterns of gene expression in M. tuberculosis in a macrophage infection model that extends from infection, through intracellular adaptation, to the establishment of a productive infection. Using a clock plasmid to measure intracellular replication and death rates over a 14-day infection and electron microscopy to define bacterial integrity, we observed an initial period of rapid replication coupled with a high death rate. This was followed by period of slowed growth and enhanced intracellular survival, leading finally to an extended period of net growth. The transcriptional profiles of M. tuberculosis reflect these physiological transitions as the bacterium adapts to conditions within its host cell. Finally, analysis with a Transcriptional Regulatory Network model revealed linked genetic networks whereby M. tuberculosis coordinates global gene expression during intracellular survival. The integration of molecular and cellular biology together with transcriptional profiling and systems analysis offers unique insights into the host-driven responses of intracellular pathogens such as M. tuberculosis.

Indexed as

Gene Expression ProfilingTuberculosisAdaptation, PhysiologicalAnimalsHost-Pathogen InteractionsIntracellular SpaceMacrophagesMiceMice, Inbred C57BLMicroarray AnalysisMicroscopy, Electron, TransmissionMycobacterium tuberculosisReal-Time Polymerase Chain Reaction

Identifiers

PMID22737072
PMCPMC3380936

What OpenQuestion holds

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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 OpenQuestion graph.