Evidence map›Paper›PMID 30217535›Full record

ArticleBrain, behavior, and immunity2018

Microglia have a protective role in viral encephalitis-induced seizure development and hippocampal damage.

Inken Waltl, Christopher Käufer, Ingo Gerhauser, Chintan Chhatbar, Luca Ghita, Ulrich Kalinke, Wolfgang Löscher

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.6field-weighted citation impact, top 3% 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, 133 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. [Therapeutic effects of inulin-type oligosaccharides ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  14. 5-HTJournal of advanced research · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. The Development of Epilepsy Following CNS Viral Infections: Mechanisms.Current neurology and neuroscience reports · 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

7 authors at 2 institutions in 1 country.

Inken WaltlDepartment of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Germany; Center for Systems Neuroscience, Hannover, Germany.
Christopher KäuferDepartment of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Germany.
Ingo GerhauserDepartment of Pathology, University of Veterinary Medicine Hannover, Germany.
Chintan ChhatbarInstitute for Experimental Infection Research, TWINCORE, Center for Experimental and Clinical Infection Research, a Joint Venture Between the Helmholtz Center for Infection Research, Braunschweig, and the Hannover Medical School, Hannover, Germany.
Luca GhitaInstitute for Experimental Infection Research, TWINCORE, Center for Experimental and Clinical Infection Research, a Joint Venture Between the Helmholtz Center for Infection Research, Braunschweig, and the Hannover Medical School, Hannover, Germany.
Ulrich KalinkeCenter for Systems Neuroscience, Hannover, Germany; Institute for Experimental Infection Research, TWINCORE, Center for Experimental and Clinical Infection Research, a Joint Venture Between the Helmholtz Center for Infection Research, Braunschweig, and the Hannover Medical School, Hannover, Germany.
Wolfgang LöscherDepartment of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Germany; Center for Systems Neuroscience, Hannover, Germany. Electronic address: wolfgang.loescher@tiho-hannover.de.
University of Veterinary Medicine Hannover, Foundation · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the central nervous system (CNS), innate immune surveillance is mainly coordinated by microglia. These CNS resident myeloid cells are assumed to help orchestrate the immune response against infections of the brain. However, their specific role in this process and their interactions with CNS infiltrating immune cells, such as blood-borne monocytes and T cells are only incompletely understood. The recent development of PLX5622, a specific inhibitor of colony-stimulating factor 1 receptor that depletes microglia, allows studying the role of microglia in conditions of brain injury such as viral encephalitis, the most common form of brain infection. Here we used this inhibitor in a model of viral infection-induced epilepsy, in which C57BL/6 mice are infected by a picornavirus (Theiler's murine encephalomyelitis virus) and display seizures and hippocampal damage. Our results show that microglia are required early after infection to limit virus distribution and persistence, most likely by modulating T cell activation. Microglia depletion accelerated the occurrence of seizures, exacerbated hippocampal damage, and led to neurodegeneration in the spinal cord, which is normally not observed in this mouse strain. This study enhances our understanding of the role of microglia in viral encephalitis and adds to the concept of microglia-T cell crosstalk.

Indexed as

AnimalsBrainCentral Nervous SystemDisease Models, AnimalEncephalitisEncephalitis, ViralEpilepsyFemaleHippocampusMacrophagesMiceMice, Inbred C57BLMicrogliaMonocytesOrganic ChemicalsSeizuresOrganic ChemicalsPLX5622HippocampusMonocytesNeuroinflammationSeizuresSpinal cordT cells

Identifiers

PMID30217535
PMCPMC7111316
OpenAlexW2891439332

What Socratic 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 Socratic graph.