Evidence map›Paper›PMID 29040326›Full record

ArticlePLoS pathogens2017

Mycobacterium tuberculosis infection modulates adipose tissue biology.

Macarena Beigier-Bompadre, Georgina N Montagna, Anja A Kühl, Laura Lozza, January Weiner, Andreas Kupz, Alexis Vogelzang, Hans-Joachim Mollenkopf, Delia Löwe, Silke Bandermann and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.3field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. International journal of molecular sciences · 2025
    Article
  5. Observational
  6. Review
  7. Tuberculosis and Increased Incidence of Cardiovascular Disease: Cohort Study Using United States and United Kingdom Health Records.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Initial immune response after exposure toFrontiers in immunology · 2023
    Review
  19. The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023
    Review
  20. Review
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

14 authors at 2 institutions in 1 country.

Macarena Beigier-BompadreDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0002-6490-5859
Georgina N MontagnaParasitology Unit, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0003-0283-8977
Anja A KühlMedical Department, Division of Gastroenterology, Infectiology and Rheumatology, Charité - University Medicine, Berlin, Germany.
Laura LozzaDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0002-7948-4954
January WeinerDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0003-1438-7819
Andreas KupzDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Alexis VogelzangDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hans-Joachim MollenkopfCore Facility, Max Planck Institute for Infection Biology, Berlin, Germany.
Delia LöweDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Silke BandermannDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Anca DorhoiDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
Volker BrinkmannCore Facility, Max Planck Institute for Infection Biology, Berlin, Germany.
Kai MatuschewskiParasitology Unit, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0001-6147-8591
Stefan H E KaufmannDepartment of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.ORCID http://orcid.org/0000-0001-9866-8268
Max Planck Institute for Infection Biology · DECharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis (Mtb) primarily resides in the lung but can also persist in extrapulmonary sites. Macrophages are considered the prime cellular habitat in all tissues. Here we demonstrate that Mtb resides inside adipocytes of fat tissue where it expresses stress-related genes. Moreover, perigonadal fat of Mtb-infected mice disseminated the infection when transferred to uninfected animals. Adipose tissue harbors leukocytes in addition to adipocytes and other cell types and we observed that Mtb infection induces changes in adipose tissue biology depending on stage of infection. Mice infected via aerosol showed infiltration of inducible nitric oxide synthase (iNOS) or arginase 1 (Arg1)-negative F4/80+ cells, despite recruitment of CD3+, CD4+ and CD8+ T cells. Gene expression analysis of adipose tissue of aerosol Mtb-infected mice provided evidence for upregulated expression of genes associated with T cells and NK cells at 28 days post-infection. Strikingly, IFN-γ-producing NK cells and Mtb-specific CD8+ T cells were identified in perigonadal fat, specifically CD8+CD44-CD69+ and CD8+CD44-CD103+ subpopulations. Gene expression analysis of these cells revealed that they expressed IFN-γ and the lectin-like receptor Klrg1 and down-regulated CD27 and CD62L, consistent with an effector phenotype of Mtb-specific CD8+ T cells. Sorted NK cells expressed higher abundance of Klrg1 upon infection, as well. Our results reveal the ability of Mtb to persist in adipose tissue in a stressed state, and that NK cells and Mtb-specific CD8+ T cells infiltrate infected adipose tissue where they produce IFN-γ and assume an effector phenotype. We conclude that adipose tissue is a potential niche for Mtb and that due to infection CD8+ T cells and NK cells are attracted to this tissue.

Indexed as

AdipocytesAdipose TissueAnimalsCD8-Positive T-LymphocytesHumansKiller Cells, NaturalMiceMycobacterium tuberculosisTuberculosisVirus Latency

Identifiers

PMID29040326
PMCPMC5695609
OpenAlexW2767088716

What OpenQuestion holds

Textmetadata
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.