Evidence map›Paper›PMID 23236276›Full record

ArticlePLoS pathogens2012

GABAergic signaling is linked to a hypermigratory phenotype in dendritic cells infected by Toxoplasma gondii.

Jonas M Fuks, Romanico B G Arrighi, Jessica M Weidner, Suresh Kumar Mendu, Zhe Jin, Robert P A Wallin, Bence Rethi, Bryndis Birnir, Antonio Barragan

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 167 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Peripheral GABA Signaling in Metabolic Adaptation and Maladaptation.International journal of molecular sciences · 2026
    Review
  4. mBio · 2026
    Article
  5. Article
  6. mBio · 2025
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Diseases Caused by and Behaviors Associated withPathogens (Basel, Switzerland) · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Prevalence ofMicroorganisms · 2024
    Article
  19. Toxoplasma-induced behavior changes - is microbial dysbiosis the missing link?Frontiers in cellular and infection microbiology · 2024
    Review
  20. Article

24 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

9 authors at 4 institutions in 1 country.

Jonas M FuksCenter for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.
Romanico B G Arrighi
Jessica M Weidner
Suresh Kumar Mendu
Zhe Jin
Robert P A Wallin
Bence Rethi
Bryndis Birnir
Antonio Barragan
Uppsala University · SEKarolinska Institutet · SEKarolinska University Hospital · SESwedish Institute · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During acute infection in human and animal hosts, the obligate intracellular protozoan Toxoplasma gondii infects a variety of cell types, including leukocytes. Poised to respond to invading pathogens, dendritic cells (DC) may also be exploited by T. gondii for spread in the infected host. Here, we report that human and mouse myeloid DC possess functional γ-aminobutyric acid (GABA) receptors and the machinery for GABA biosynthesis and secretion. Shortly after T. gondii infection (genotypes I, II and III), DC responded with enhanced GABA secretion in vitro. We demonstrate that GABA activates GABA(A) receptor-mediated currents in T. gondii-infected DC, which exhibit a hypermigratory phenotype. Inhibition of GABA synthesis, transportation or GABA(A) receptor blockade in T. gondii-infected DC resulted in impaired transmigration capacity, motility and chemotactic response to CCL19 in vitro. Moreover, exogenous GABA or supernatant from infected DC restored the migration of infected DC in vitro. In a mouse model of toxoplasmosis, adoptive transfer of infected DC pre-treated with GABAergic inhibitors reduced parasite dissemination and parasite loads in target organs, e.g. the central nervous system. Altogether, we provide evidence that GABAergic signaling modulates the migratory properties of DC and that T. gondii likely makes use of this pathway for dissemination. The findings unveil that GABA, the principal inhibitory neurotransmitter in the brain, has activation functions in the immune system that may be hijacked by intracellular pathogens.

Indexed as

AnimalsCell MovementCells, CulturedChemokine CCL19Dendritic Cellsgamma-Aminobutyric AcidHumansMiceReceptors, GABA-ASignal TransductionToxoplasmaToxoplasmosisCCL19 protein, humanCcl19 protein, mouseChemokine CCL19gamma-Aminobutyric AcidReceptors, GABA-A

Identifiers

PMID23236276
PMCPMC3516538
OpenAlexW2144924711

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.