Evidence map›Paper›PMID 23391218›Full record

ArticleBMC neuroscience2013

Absence of CCR5 increases neutrophil recruitment in severe herpetic encephalitis.

Márcia Carvalho Vilela, Graciela Kunrath Lima, David Henrique Rodrigues, Norinne Lacerda-Queiroz, Vinicius Sousa Pietra Pedroso, Aline Silva Miranda, Milene Alvarenga Rachid, Erna Geessien Kroon, Marco Antônio Campos, Mauro Martins Teixeira and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Insights into the pathogenesis of herpes simplex encephalitis from mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
  6. Platelet Activating Factor (PAF) Receptor Deletion or Antagonism Attenuates Severe HSV-1 Meningoencephalitis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  7. Article
  8. Article
  9. Article
  10. Targeting CCL5 in inflammation.Expert opinion on therapeutic targets · 2013
    Review
  11. Article
  12. Review
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

12 authors at 4 institutions in 3 countries.

Márcia Carvalho VilelaPós-Graduação em Ciências da Saúde, Infectologia e Medicina Tropical, Laboratório de Imunofarmacologia, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Av Antonio Carlos, 6627 Pampulha, Belo Horizonte, MG 31270-901, Brazil. marciacvilela@gmail.com
Graciela Kunrath Lima
David Henrique Rodrigues
Norinne Lacerda-Queiroz
Vinicius Sousa Pietra Pedroso
Aline Silva Miranda
Milene Alvarenga Rachid
Erna Geessien Kroon
Marco Antônio Campos
Mauro Martins Teixeira
Johann Sellner
Antonio Lucio Teixeira
Universidade Federal de Minas Gerais · BRChristian Doppler Klinik · ATFundação Oswaldo Cruz · BRUniversidade Federal de Viçosa · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe neuroinflammatory response aimed at clearance of herpes simplex virus-1 (HSV-1) plays a key role in the pathogenesis of neuroaxonal damage in herpetic encephalitis. Leukocytes activated in an adaptive immune response access brain tissue by passing through the blood-brain barrier. The chemokine CCL5/RANTES is involved in recruitment of these cells to the brain acting via the receptors CCR1, CCR3 and mainly CCR5. Here, we evaluated the role of CCR5 on traffic of leukocytes in the brain microvasculature, cellular and cytokines profile in a severe form of herpetic encephalitis.

resultsWild type and mice lacking CCR5 (CCR5-/-) were inoculated intracerebrally with 104 PFU of neurotropic HSV-1. We evaluated the traffic of leukocytes in the brain microvasculature using intravital microscopy and the profile of cytokines by Enzyme-Linked Immunosorbent Assay at 1 day post infection. Flow cytometry and histopathological analyses were also carried out in brain tissue. Absence of CCR5 leads to lower viral load and an increased leukocyte adhesion in brain microvasculature, predominantly of neutrophils (CD11+ Ly6G+ cells). Moreover, there was a significant increase in the levels of MIP-1/CCL2, RANTES/CCL5, KC/CXCL1 and MIG/CXCL9 in the brain of infected CCR5-/- mice.

conclusionsThese results suggest that the absence of CCR5 may boost the immune response with a high neutrophil recruitment which most likely helps in viral clearance. Nonetheless, the elevated immune response may be detrimental to the host.

Indexed as

AnimalsAntigens, LyBrainCell AdhesionCytokinesDisease Models, AnimalEncephalitis, Herpes SimplexEnzyme-Linked Immunosorbent AssayFlow CytometryGene Expression RegulationLeukocytesMiceMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationReceptors, CCR5Antigens, LyCytokinesLy6G antigen, mouseReceptors, CCR5

Identifiers

PMID23391218
PMCPMC3618319
OpenAlexW2040055625

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.