CoChat
Sign Up
Cited by 105Tuberculosis Research and EpidemiologyImmune responses and vaccinationsInfectious Diseases and Tuberculosis

M. tuberculosis Induces Potent Activation of IDO-1, but This Is Not Essential for the Immunological Control of Infection

Open access
Blumenthal, Antje, Nagalingam, Gayathri, Huch, Jennifer H., Walker, Lara, Guillemin, Gilles J., Smythe, George A., Ehrt, Sabine, Britton, Warwick J. +1 more·2012·PLoS ONE
DOI 10.1371/journal.pone.0037314PMC PMC3359358
Open this paper in CoChat — free accountOpen PDF

Abstract

Indoleamine 2,3-dioxygenesae-1 (IDO-1) catalyses the initial, rate-limiting step in tryptophan metabolism, thereby regulating tryptophan availability and the formation of downstream metabolites, including picolinic and quinolinic acid. We found that Mycobacterium tuberculosis infection induced marked upregulation of IDO-1 expression in both human and murine macrophages in vitro and in the lungs of mice following aerosol challenge with M. tuberculosis. The absence of IDO-1 in dendritic cells enhanced the activation of mycobacteria-specific T cells in vitro. Interestingly, IDO-1-deficiency during M. tuberculosis infection in mice was not associated with altered mycobacteria-specific T cell responses in vivo. The bacterial burden of infected organs, pulmonary inflammatory responses, and survival were also comparable in M. tuberculosis-infected IDO-1 deficient and wild type animals. Tryptophan is metabolised into either picolinic acid or quinolinic acid, but only picolinic acid inhibited the growth of M. tuberculosis in vitro. By contrast macrophages infected with pathogenic mycobacteria, produced quinolinic, rather than picolinic acid, which did not reduce M. tuberculosis growth in vitro. Therefore, although M. tuberculosis induces robust expression of IDO-1 and activation of tryptophan metabolism, IDO-1-deficiency fails to impact on the immune control and the outcome of the infection in the mouse model of tuberculosis.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1371/journal.pone.0037314

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In the setting of M. tuberculosis infection, IDO activation appears to be ineffective in controlling the infection.

    “However, in the setting of M. tuberculosis infection, IDO activation appears to be ineffective in controlling the infection.”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]

  • IDO deficient mice control M. tuberculosis infection as well as wildtype animals, and lack of IDO does not affect mycobacterial specific T-cell responses.

    “IDO deficient mice were able to control M. tuberculosis infection as good as wildtype animals and lack of IDO did not affect mycobacterial specific T-cell responses (96).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]

  • Tryptophan is essential for M. tuberculosis growth.

    “Tryptophan is essential for M. tuberculosis growth, however, IDO deficient mice were able to control M. tuberculosis infection as good as wildtype animals and lack of IDO did not affect mycobacterial specific T-cell responses (96).”

    From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [96]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

1 of the 55 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. [6]MacKenzie CR Langen R Takikawa O Daubener W 1999 Inhibition of indoleamine 2,3-dioxygenase in human macrophages inhibits interferon-gamma-induced bacteriostasis but does not abrogate toxoplasmastasis. Eur J Immunol 29 3254 3261 10540337
  2. [20]Demangel C Bean AG Martin E Feng CG Kamath AT 1999 Protection against aerosol Mycobacterium tuberculosis infection using Mycobacterium bovis Bacillus Calmette Guerin-infected dendritic cells. Eur J Immunol 29 1972 1979 10382760

Cited by

Sorted by citations

Related

Authors
Blumenthal, A., Nagalingam, G., Huch, J. H., Walker, L., Guillemin, G. J., Smythe, G. A., Ehrt, S., Britton, W. J., & Saunders, B. M.
Affiliations
  • The University of Queensland (AU)
  • Centenary Institute (AU)
  • UNSW Sydney (AU)
  • Cornell University (US)
  • The University of Sydney (AU)
Corresponding author
  • Blumenthal, Antje
  • Saunders, Bernadette M.
ORCID
Venue
PLoS ONE
Publisher
Public Library of Science (PLoS)
Published
2012-05-23
Volume
7
Issue
5
Pages
e37314
ISSN
1932-6203 (ISSN-L)
DOI
10.1371/journal.pone.0037314
PMC
PMC3359358
OpenAlex
W2025969665
Cited by
105
References
55
Citations by year
2026: 4 · 2025: 3 · 2024: 7 · 2023: 7 · 2022: 6 · 2021: 10 · 2020: 14 · 2019: 7 · 2018: 10 · 2017: 7 · 2016: 6 · 2015: 11 · 2014: 6 · 2013: 5 · 2012: 2
FWCI
5.30
Type
journal article
Language
en
Open access
Licence
Locations
  • PLoS ONE (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Figshare (submittedVersion, cc-by)
  • UTS ePRESS (University of Technology Sydney) (submittedVersion)
Funders
  • National Institutes of Health
  • Medical Research Council
  • National Health and Medical Research Council
  • National Heart, Lung, and Blood Institute (R01HL068525, HL68525)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
  • Health Sciences › Medicine › Surgery › Infectious Diseases and Tuberculosis
Keywords
Mycobacterium tuberculosis, IDO1, tryptophan metabolism, tryptophan catabolism, picolinic acid, quinolinic acid, macrophages, dendritic cells, tuberculosis immunology, bacterial growth inhibition
MeSH terms
Animals, Female, Humans, Immunohistochemistry, Lung, Macrophages, Mice, Inbred C57BL, Mycobacterium tuberculosis, Picolinic Acids, T-Lymphocytes, Tryptophan, Tuberculosis, Blotting, Western, DNA Primers, Mice, Knockout, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Microarray Analysis, Indoleamine-Pyrrole 2,3,-Dioxygenase, Mice, Kaplan-Meier Estimate, Real-Time Polymerase Chain Reaction

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review