Evidence map›Paper›PMID 31559534›Full record

ArticleNeuromolecular medicine2020

Intravenous Immunoglobulin (IVIg) Induce a Protective Phenotype in Microglia Preventing Neuronal Cell Death in Ischaemic Stroke.

Vivien Häußler, Tristan Daehn, Björn Rissiek, Vanessa Roth, Christian Gerloff, Thiruma V Arumugam, Tim Magnus, Mathias Gelderblom

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

8 citing papers in PubMed, 24 citations in OpenAlex.

  1. ZnBalkan medical journal · 2024
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Potential microglia-based interventions for stroke.CNS neuroscience & therapeutics · 2020
    Review
  8. 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

8 authors at 3 institutions in 2 countries.

Vivien HäußlerDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Tristan DaehnDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Björn RissiekDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Vanessa RothDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Christian GerloffDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Thiruma V ArumugamDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Tim MagnusDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany.
Mathias GelderblomDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Martinistraße 52, 20246, Hamburg, Germany. m.gelderblom@uke.de.
University Medical Center Hamburg-Eppendorf · DENational University of Singapore · SGUniversität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting the immune system and thereby modulating the inflammatory response in ischemic stroke has shown promising therapeutic potential in various preclinical trials. Among those, intravenous immunoglobulins (IVIg) have moved into the focus of attention. In a murine model of experimental stroke, we explored the therapeutic potential of IVIg on the neurological outcome and the inflammatory response. Further, we used an in vitro system to assess effects of IVIg-stimulated microglia on neuronal survival. Treatment with IVIg resulted in decreased lesion sizes, without significant effects on the infiltration and activation pattern of peripheral immune cells. However, in microglia IVIg induced a switch towards an upregulation of protective polarization markers, and the ablation of microglia led to the loss of neuroprotective IVIg effects. Functionally, IVIg stimulated microglia ameliorated neuronal cell death elicited by oxygen and glucose deprivation in vitro. Notably, application of IVIg in vivo led to a comparable decrease of apoptotic neurons in the penumbra area. Although neuroprotective effects of IVIg in vivo and in vitro have been established in previous studies, we were able to show for the first time, that IVIg modulates the polarization of microglia during the pathogenesis of stroke.

Indexed as

AnimalsApoptosisCell PolarityCells, CulturedGlucoseImmunoglobulins, IntravenousInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLMicrogliaNeuronsNeuroprotective AgentsNeutrophil InfiltrationOxygenPhenotypeGlucoseImmunoglobulins, IntravenousNeuroprotective AgentsOxygenIntravenous immunoglobulins (IVIg)Ischemic strokeMicrogliaMiddle cerebral artery occlusion (MCAO)Sterile inflammation

Identifiers

PMID31559534
OpenAlexW2975425165

What OpenQuestion holds

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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.