Evidence map›Paper›PMID 20940264›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

Role of CCR5 and its ligands in the control of vascular inflammation and leukocyte recruitment required for acute excitotoxic seizure induction and neural damage.

Jean-Pierre Louboutin, Alena Chekmasova, Elena Marusich, Lokesh Agrawal, David S Strayer

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 78 citations in OpenAlex.

  1. Review
  2. CCR5 predicts neurotoxicity in CAR-T-cell therapy.British journal of haematology · 2025
    Article
  3. Article
  4. Review
  5. Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Immune Alterations in CD8Molecular neurobiology · 2018
    Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Jean-Pierre LouboutinDepartment of Pathology, Jefferson Medical College, 1020 Locust St., Rm. 251, Philadelphia, PA 19107, USA. jplouboutin@hotmail.com
Alena Chekmasova
Elena Marusich
Lokesh Agrawal
David S Strayer
Thomas Jefferson University · US

Funding

Targeting HIV infection of the cns using gene deliveryR01MH070287 · NIMH · THOMAS JEFFERSON UNIVERSITY · PI STRAYER, DAVID S · 2004 to 2008
$1.9M
NIMH NIH HHS MH70287NIMH NIH HHS R01 MH070287
6 · The paper itself

Abstract

Chemokines may play a role in leukocyte migration across the blood-brain barrier (BBB) during neuroinflammation and other neuropathological processes, such as epilepsy. We investigated the role of the chemokine receptor CCR5 in seizures. We used a rat model based on intraperitoneal kainic acid (KA) administration. Four months before KA injection, adult rats were given femoral intramarrow inoculations of SV (RNAiR5-RevM10.AU1), which carries an interfering RNA (RNAi) against CCR5, plus a marker epitope (AU1), or its monofunctional RNAi-carrying homologue, SV(RNAiR5). This treatment lowered expression of CCR5 in circulating cells. In control rats, seizures induced elevated expression of CCR5 ligands MIP-1α and RANTES in the microvasculature, increased BBB leakage and CCR5(+) cells, as well as neuronal loss, inflammation, and gliosis in the hippocampi. Animals given either the bifunctional or the monofunctional vector were largely protected from KA-induced seizures, neuroinflammation, BBB damage, and neuron loss. Brain CCR5 mRNA was reduced. Rats receiving RNAiR5-bearing vectors showed far greater repair responses: increased neuronal proliferation, and decreased production of MIP-1α and RANTES. Controls received unrelated SV(BUGT) vectors. Decrease in CCR5 in circulating cells strongly protected from excitotoxin-induced seizures, BBB leakage, CNS injury, and inflammation, and facilitated neurogenic repair.

Indexed as

AnimalsBlood-Brain BarrierBrainChemokine CCL3Chemokine CCL5FemaleGene Expression RegulationGliosisHippocampusKainic AcidLigandsNeuronsNeurotoxinsRatsRats, Sprague-DawleyReceptors, CCR5Chemokine CCL3Chemokine CCL5Kainic AcidLigandsNeurotoxinsReceptors, CCR5

Identifiers

PMID20940264
PMCPMC3023386
OpenAlexW1977477970

What OpenQuestion 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 OpenQuestion graph.