Evidence map›Paper›PMID 27109609›Full record

ArticleBrain, behavior, and immunity2016

Cerebral complement C1q activation in chronic Toxoplasma infection.

Jianchun Xiao, Ye Li, Kristin L Gressitt, Helen He, Geetha Kannan, Tracey L Schultz, Nadezhda Svezhova, Vern B Carruthers, Mikhail V Pletnikov, Robert H Yolken and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain, behavior, and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular Mimicry BetweenInternational journal of molecular sciences · 2025
    Article
  4. Review
  5. Innate Immune Mechanisms in the Central Nervous System.Advances in experimental medicine and biology · 2025
    Review
  6. Frontiers in cellular and infection microbiology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Toxoplasma-induced behavior changes - is microbial dysbiosis the missing link?Frontiers in cellular and infection microbiology · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Foods (Basel, Switzerland) · 2022
    Review
  16. Article
  17. Review
  18. Comprehensive Overview ofPathogens (Basel, Switzerland) · 2021
    Review
  19. Review
  20. Heliyon · 2021
    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

11 authors at 3 institutions in 1 country.

Jianchun XiaoStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Ye LiStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Kristin L GressittStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Helen HeStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Geetha KannanDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Tracey L SchultzDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Nadezhda SvezhovaDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Vern B CarruthersDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Mikhail V PletnikovDepartment of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Robert H YolkenStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA.
Emily G SeveranceStanley Division of Developmental Neurovirology, Department of Pediatrics, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1105, Baltimore, MD 21287-4933, USA. Electronic address: eseverance@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · USUniversity of Michigan–Ann Arbor · US

Funding

Project 3P50MH094268 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SAWA, AKIRA · 2011 to 2020
$19.9M
Mutant DISC 1 and Abnormal Neurodevelopment in Mental IllnessR01MH083728 · NIMH · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI PLETNIKOV, MIKHAIL V · 2009 to 2020
$4.9M
NIMH NIH HHS P50 MH094268NIMH NIH HHS R01 MH083728
6 · The paper itself

Abstract

Exposure to the neurotropic parasite, Toxoplasma gondii, causes significant brain and behavioral anomalies in humans and other mammals. Understanding the cellular mechanisms of T. gondii-generated brain pathologies would aid the advancement of novel strategies to reduce disease. Complement factor C1q is part of a classic immune pathway that functions peripherally to tag and remove infectious agents and cellular debris from circulation. In the developing and adult brain, C1q modifies neuronal architecture through synapse marking and pruning. T. gondii exposure and complement activation have both been implicated in the development of complex brain disorders such as schizophrenia. Thus, it seems logical that mechanistically, the physiological pathways associated with these two factors are connected. We employed a rodent model of chronic infection to investigate the extent to which cyst presence in the brain triggers activation of cerebral C1q. Compared to uninfected mice, cortical C1q was highly expressed at both the RNA and protein levels in infected animals bearing a high cyst burden. In these mice, C1q protein localized to cytoplasm, adjacent to GFAP-labeled astrocytes, near degenerating cysts, and in punctate patterns along processes. In summary, our results demonstrated an upregulation of cerebral C1q in response to latent T. gondii infection. Our data preliminarily suggest that this complement activity may aid in the clearance of this parasite from the CNS and in so doing, have consequences for the connectivity of neighboring cells and synapses.

Indexed as

AnimalsCerebral CortexChronic DiseaseComplement C1qCystsFemaleMiceToxoplasmosisComplement C1qGliaMAG1 antibodiesNeuronsPrefrontal cortexPsychiatryToxoplasmosis

Identifiers

PMID27109609
PMCPMC5067173
OpenAlexW2339662611

What OpenQuestion holds

Textmetadata
LicenceTDM
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.