Evidence map›Paper›PMID 20385761›Full record

ArticleInfection and immunity2010

Indoleamine 2,3-dioxygenase 1 is a lung-specific innate immune defense mechanism that inhibits growth of Francisella tularensis tryptophan auxotrophs.

Kaitian Peng, Denise M Monack

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Frontiers in cellular and infection microbiology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Kynurenine Pathway in Respiratory Diseases.International journal of tryptophan research : IJTR · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Allosteric inhibitors of Mycobacterium tuberculosis tryptophan synthase.Protein science : a publication of the Protein Society · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Kaitian PengDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California, USA.
Denise M Monack
Stanford University · US

Funding

Vaccines and Diagnostics TrialsU54AI065359 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARBOUR, ALAN G. · 2005 to 2013
$88.8M
The role of Listeria cyclic-di-AMP during infection and immunityP01AI063302 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI STANLEY, SARAH A · 2004 to 2025
$45.5M
NIAID NIH HHS AI063302NIAID NIH HHS AI065359NIAID NIH HHS P01 AI063302NIAID NIH HHS U54 AI065359
6 · The paper itself

Abstract

Upon microbial challenge, organs at various anatomic sites of the body employ different innate immune mechanisms to defend against potential infections. Accordingly, microbial pathogens evolved to subvert these organ-specific host immune mechanisms to survive and grow in infected organs. Francisella tularensis is a bacterium capable of infecting multiple organs and thus encounters a myriad of organ-specific defense mechanisms. This suggests that F. tularensis may possess specific factors that aid in evasion of these innate immune defenses. We carried out a microarray-based, negative-selection screen in an intranasal model of Francisella novicida infection to identify Francisella genes that contribute to bacterial growth specifically in the lungs of mice. Genes in the bacterial tryptophan biosynthetic pathway were identified as being important for F. novicida growth specifically in the lungs. In addition, a host tryptophan-catabolizing enzyme, indoleamine 2,3-dioxygenase 1 (IDO1), is induced specifically in the lungs of mice infected with F. novicida or Streptococcus pneumoniae. Furthermore, the attenuation of F. novicida tryptophan mutant bacteria was rescued in the lungs of IDO1(-/-) mice. IDO1 is a lung-specific innate immune mechanism that controls pulmonary Francisella infections.

Indexed as

AnimalsBiosynthetic PathwaysCell LineColony Count, MicrobialFemaleFrancisella tularensisGene Expression ProfilingIndoleamine-Pyrrole 2,3,-DioxygenaseLungMacrophagesMiceMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisSpleenStreptococcus pneumoniaeIndoleamine-Pyrrole 2,3,-DioxygenaseTryptophanVirulence Factors

Identifiers

PMID20385761
PMCPMC2876573
OpenAlexW2147011854

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.