Evidence map›Paper›PMID 25178113›Full record

ArticleJournal of neuroinflammation2014

Dynamics of major histocompatibility complex class II-positive cells in the postischemic brain--influence of levodopa treatment.

Enida Kuric, Karsten Ruscher

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
  7. Article
  8. Glia-immune interactions post-ischemic stroke and potential therapies.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  9. Article
  10. The role of dopaminergic immune cell signalling in poststroke inflammation.Therapeutic advances in neurological disorders · 2018
    Review
  11. Article
  12. Review
  13. Article
  14. Clinical Trials of Immunomodulation in Ischemic Stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  15. Article
  16. Article
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

2 authors at 1 institution in 1 country.

Enida KuricLaboratory for Experimental Brain Research, Division of Neurosurgery, Department of Clinical Sciences, Lund University, BMC A13, Lund, S-22184, Sweden. enida.kuric@med.lu.se.
Karsten Ruscher
Lund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebral ischemia activates both the innate and the adaptive immune response, the latter being activated within days after the stroke onset and triggered by the recognition of foreign antigens.

methodsIn this study we have investigated the phenotype of antigen presenting cells and the levels of associated major histocompatibility complex class II (MHC II) molecules in the postischemic brain after transient occlusion of the middle cerebral artery (tMCAO) followed by levodopa/benserazide treatment. Male Sprague Dawley rats were subjected to tMCAO for 105 minutes and received levodopa (20 mg/kg)/benserazide (15 mg/kg) for 5 days starting on day 2 after tMCAO. Thereafter, immune cells were isolated from the ischemic and contralateral hemisphere and analyzed by flow cytometry. Complementarily, the spatiotemporal profile of MHC II-positive (MHC II(+)) cells was studied in the ischemic brain during the first 30 days after tMCAO; protein levels of MHC II and the levels of inflammation associated cytokines were determined in the ischemic hemisphere.

resultsWe found that microglia/macrophages represent the main MHC II expressing cell in the postischemic brain one week after tMCAO. No differences in absolute cell numbers were found between levodopa/benserazide and vehicle-treated animals. In contrast, MHC II protein levels were significant downregulated in the ischemic infarct core by levodopa/benserazide treatment. This reduction was accompanied by reduced levels of IFN-γ, TNF-α and IL-4 in the ischemic hemisphere. In the contralateral hemisphere, we exclusively detected MHC II(+) cells in the corpus callosum. Interestingly, the number of cells was increased by treatment with levodopa/benserazide independent from the infarct size 14 days after tMCAO.

conclusionsResults suggest that dopamine signaling is involved in the adaptive immune response after stroke and involves microglia/macrophages.

Indexed as

AnimalsAntigen-Presenting CellsBenserazideBrainCytokinesDisease Models, AnimalDopamine AgentsDrug CombinationsFlow CytometryFunctional LateralityHistocompatibility Antigens Class IIInfarction, Middle Cerebral ArteryLevodopaMacrophagesMaleMicrogliaBenserazidebenserazide, levodopa drug combinationCytokinesDopamine AgentsDrug CombinationsHistocompatibility Antigens Class IILevodopa

Identifiers

PMID25178113
PMCPMC4149192
OpenAlexW2103038534

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.