Evidence map›Paper›PMID 27634961›Full record

ArticleJournal of neuropathology and experimental neurology2016

Molecular and Cellular Responses to Interleukin-4 Treatment in a Rat Model of Transient Ischemia.

Starlee Lively, Sarah Hutchings, Lyanne C Schlichter

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

Article in Journal of neuropathology and experimental neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke.Current neurology and neuroscience reports · 2023
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Attack of the Clones: Microglia in Health and Disease.Frontiers in cellular neuroscience · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
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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

3 authors at 1 institution in 1 country.

Starlee LivelyFrom the Krembil Research Institute, University Health Network, Toronto, ON, Canada (SL, SH, LCS); Department of Physiology, University of Toronto, Toronto, ON, Canada (SH, LCS).
Sarah HutchingsFrom the Krembil Research Institute, University Health Network, Toronto, ON, Canada (SL, SH, LCS); Department of Physiology, University of Toronto, Toronto, ON, Canada (SH, LCS).
Lyanne C SchlichterFrom the Krembil Research Institute, University Health Network, Toronto, ON, Canada (SL, SH, LCS); Department of Physiology, University of Toronto, Toronto, ON, Canada (SH, LCS).
Krembil Research Institute

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Within hours after stroke, potentially cytotoxic pro-inflammatory mediators are elevated within the brain; thus, one potential therapeutic strategy is to reduce them and skew the brain toward an anti-inflammatory state. Because interleukin-4 (IL-4) treatment induces an anti-inflammatory, "alternative-activation" state in microglia and macrophages in vitro, we tested the hypothesis that early supplementation of the brain with IL-4 can shift it toward an anti-inflammatory state and reduce damage after transient focal ischemia. Adult male rat striata were injected with endothelin-1, with or without co-injection of IL-4. Inflammation, glial responses and damage to neurons and white matter were quantified from 1 to 7 days later. At 1 day, IL-4 treatment increased striatal expression of several anti-inflammatory markers (ARG1, CCL22, CD163, PPARγ), increased phagocytic (Iba1-positive, CD68-positive) microglia/macrophages, and increased VEGF-A-positive infiltrating neutrophils in the infarcts. At 7 days, there was evidence of sustained, propagating responses. IL-4 increased CD206, CD200R1, IL-4Rα, STAT6, PPARγ, CD11b, and TLR2 expression and increased microglia/macrophages in the infarct and astrogliosis outside the infarct. Neurodegeneration and myelin damage were not reduced, however. The sustained immune and glial responses when resolution and repair processes have begun warrant further studies of IL-4 treatment regimens and long-term outcomes.

Indexed as

Alternative activationGliosisInterleukin 4NeuroinflammationNeutrophil entryPhagocytic microgliaTransient brain ischemia.

Identifiers

PMID27634961
PMCPMC5070459
OpenAlexW2518953525

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.