Evidence map›Paper›PMID 10583589›Full record

ArticleImmunology1999

Granuloma formation is required to contain bacillus growth and delay mortality in mice chronically infected with Mycobacterium tuberculosis.

B M Saunders, A A Frank, I M Orme

Open access · greenAbstract read
In one paragraph

Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
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, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. AllCurrent research in immunology · 2022
    Review
  5. Review
  6. Review
  7. Immune Response and Apoptosis-Related Pathways Induced byPathogens (Basel, Switzerland) · 2021
    Article
  8. Article
  9. Modulation of Roquin Function in Myeloid Cells ReducesJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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

3 authors at 1 institution in 1 country.

B M SaundersMycobacteria Research Laboratories, Department of Microbiology, Colorado State University, Fort Collins 80523, USA.
A A Frank
I M Orme
Colorado State University · US

Funding

CHRONIC TUBERCULOSIS--LATENT OR DYNAMICR01AI044072 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · PI ORME, IAN M · 1999 to 2008
$2.7M
DEFINED NATIVE ANTIGENS AND IMMUNITY TO TUBERCULOSISR01AI040488 · NIAID · COLORADO STATE UNIVERSITY-FORT COLLINS · PI ORME, IAN M · 1996 to 2006
$1.6M
NIAID NIH HHS AI-40488NIAID NIH HHS AI-44072NIAID NIH HHS R01 AI040488NIAID NIH HHS R01 AI044072
6 · The paper itself

Abstract

Previous studies in this laboratory have shown that mice with a gene disruption to the intracellular adhesion molecule-1 (ICAM-K/O) express normal cell-mediated immunity but cannot mount delayed-type hypersensitivity reactions following Mycobacterium tuberculosis infection. However, even in the absence of any appreciable granuloma formation, these mice control bacterial growth for at least 90 days. While not required to control the infection initially, we hypothesized that granuloma formation was required to control chronic infection, acting by surrounding infected cells to prevent bacterial dissemination. To test this, ICAM-1 knockout mice were infected with a low dose aerosol of M. tuberculosis Erdman and were found to succumb to infection 136+/-30 days later, displaying highly elevated bacterial loads compared to wild-type mice. Lung tissue from ICAM-K/O mice displayed extensive cellular infiltration and widespread tissue necrosis, but no organized granulomatous lesions were evident, whereas the control mice displayed organized compact granulomas. These data demonstrate that while a granulomatous response is not required initially to control M. tuberculosis infection, absence of granulomas during chronic infection leads to increased bacterial growth and host death. Thus these data support the hypothesis that granuloma formation is required to control chronic infection, acting by surrounding and walling off sites of infection to prevent bacterial dissemination and maintain a state of chronic infection.

Indexed as

AnimalsChronic DiseaseColony Count, MicrobialFemaleGranulomaHypersensitivity, DelayedIntercellular Adhesion Molecule-1LungMiceMice, Inbred C57BLMice, KnockoutMycobacterium tuberculosisTuberculosisIntercellular Adhesion Molecule-1

Identifiers

PMID10583589
PMCPMC2326942
OpenAlexW1966117438

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.