Evidence map›Paper›PMID 23086406›Full record

ArticleAutophagy2013

Autophagy restricts Chlamydia trachomatis growth in human macrophages via IFNG-inducible guanylate binding proteins.

Munir A Al-Zeer, Hesham M Al-Younes, Daniel Lauster, Mohammad Abu Lubad, Thomas F Meyer

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

75 citing papers in PubMed, 114 citations in OpenAlex.

  1. Review
  2. Article
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  5. Infection and immunity · 2026
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  8. Recognition ofInfection and immunity · 2024
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  9. Review
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  11. Article
  12. Article
  13. Review
  14. Review
  15. Autophagy: the misty lands ofFrontiers in cellular and infection microbiology · 2024
    Review
  16. Vitamin D effects onFrontiers in cellular and infection microbiology · 2024
    Article
  17. Article
  18. Review
  19. Review
  20. Article

15 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 at 2 institutions in 2 countries.

Munir A Al-ZeerDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.
Hesham M Al-Younes
Daniel Lauster
Mohammad Abu Lubad
Thomas F Meyer
Max Planck Institute for Infection Biology · DEUniversity of Jordan · JO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon γ (IFNG) is a key host response regulator of intracellular pathogen replication, including that of Chlamydia spp The antichlamydial functions of IFNG manifest in a strictly host, cell-type and chlamydial strain dependent manner. It has been recently shown that the IFNG-inducible family of immunity-related GTPases (IRG) proteins plays a key role in the defense against nonhost adapted chlamydia strains in murine epithelial cells. In humans, IFN-inducible guanylate binding proteins (hGBPs) have been shown to potentiate the antichlamydial effect of IFNG; however, how hGBPs regulate this property of IFNG is unknown. In this study, we identified hGBP1/2 as important resistance factors against C. trachomatis infection in IFNG-stimulated human macrophages. Exogenous IFNG reduced chlamydial infectivity by 50 percent in wild-type cells, whereas shRNA hGBP1/2 knockdown macrophages fully supported chlamydial growth in the presence of exogenous IFNG. hGBP1/2 were recruited to bacterial inclusions in human macrophages upon stimulation with IFNG, which triggered rerouting of the typically nonfusogenic bacterial inclusions for lysosomal degradation. Inhibition of lysosomal activity and autophagy impaired the IFNG-mediated elimination of inclusions. Thus, hGBP1/2 are critical effectors of antichlamydial IFNG responses in human macrophages. Through their capacity to remodel classically nonfusogenic chlamydial inclusions and stimulate fusion with autophagosomes, hGBP1/2 disable a major chlamydial virulence mechanism and contribute to IFNG-mediated pathogen clearance.

Indexed as

AutophagyAutophagy-Related Protein 12Cell CommunicationCell LineChlamydia trachomatisGene Knockdown TechniquesGTP-Binding ProteinsHumansInclusion BodiesInterferon-gammaMacrophagesSmall Ubiquitin-Related Modifier ProteinsVirulenceATG12 protein, humanAutophagy-Related Protein 12GBP1 protein, humanGBP2 protein, humanGTP-Binding ProteinsIFNG protein, humanInterferon-gammaSmall Ubiquitin-Related Modifier Proteins

Identifiers

PMID23086406
PMCPMC3542218
OpenAlexW1966591175

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.