Evidence map›Paper›PMID 18046731›Full record

ArticleGlia2008

Modulation of innate immunity by copolymer-1 leads to neuroprotection in murine HIV-1 encephalitis.

Santhi Gorantla, Jianuo Liu, Tong Wang, Adelina Holguin, Hannah M Sneller, Huanyu Dou, Jonathan Kipnis, Larisa Poluektova, Howard E Gendelman

Abstract read
In one paragraph

Article in Glia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. FTY720 mediates activation suppression and G(0)/G (1) cell cycle arrest in a concanavalin A-induced mouse lymphocyte pan-activation model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Neuroprotective activities of CEP-1347 in models of neuroAIDS.Journal of immunology (Baltimore, Md. : 1950) · 2010
    Article
  9. Review
  10. NanoART, neuroAIDS and CNS drug delivery.Nanomedicine (London, England) · 2009
    Review
  11. Article
  12. Article
  13. 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

9 authors at 1 institution in 1 country.

Santhi GorantlaCenter for Neurovirology and Neurodegenerative Disorders, University of Nebraska Medical Center, Omaha, Nebraska 68198-5880, USA.
Jianuo Liu
Tong Wang
Adelina Holguin
Hannah M Sneller
Huanyu Dou
Jonathan Kipnis
Larisa Poluektova
Howard E Gendelman
University of Nebraska Medical Center · US

Funding

VIRAL SHUTOFF OF HOST TRANSCRIPTION--PBCV-1 INFECTEDP20RR015635 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI WOOD, CHARLES · 2000 to 2009
$22.1M
Targeted Neuro Protection of HIV-1 Associated Neurologic DiseaseP01MH064570 · NIMH · UNIVERSITY OF ROCHESTER · PI GELBARD, HARRIS A · 2001 to 2014
$19.4M
Proteomics CoreP01NS043985 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ZHENG, JIALIN CHARLES · 2003 to 2012
$11.8M
Blood Brain Barrier Physiology and HIV DementiaR37NS036126 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E. · 2001 to 2007
$2.7M
Dopamine Systems and Neuropsychiatric Changes in HIV/AIDSR01MH079886 · NIMH · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GELMAN, BENJAMIN B. · 2006 to 2010
$1.2M
Training Program in NeurovirologyT32NS007488 · NINDS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GENDELMAN, HOWARD E. · 2002 to 2006
$776k
NCRR NIH HHS P20 RR015635NCRR NIH HHS P20RR15635NIMH NIH HHS P01 MH064570NIMH NIH HHS P01 MH64570NIMH NIH HHS R01 MH079886NIMH NIH HHS R01 MH79886NINDS NIH HHS 1T32 NS07488NINDS NIH HHS 2R37 NS36136NINDS NIH HHS P01 NS043985NINDS NIH HHS P01 NS43985NINDS NIH HHS R37 NS036126NINDS NIH HHS T32 NS007488
6 · The paper itself

Abstract

Virus-infected and immune-competent mononuclear phagocytes (MP; perivascular macrophages and microglia) drive the neuropathogenesis of human immunodeficiency virus type 1 (HIV-1) infection. Modulation of the MP phenotype from neurodestructive to neuroprotective underlies adjunctive therapeutic strategies for human disease. We reasoned that, as Copolymer-1 (Cop-1) can induce neuroprotective activities in a number of neuroinflammatory and neurodegenerative disorders, it could directly modulate HIV-1-infected MP neurotoxic activities. We now demonstrate that, in laboratory assays, Cop-1-stimulated virus-infected human monocyte-derived macrophages (MDM) protect against neuronal injury. Severe combined immune-deficient (SCID) mice were stereotactically injected with HIV-1-infected human MDM, into the basal ganglia, to induce HIV-1 encephalitis (HIVE). Cop-1 was administered subcutaneously for 7 days. In HIVE mice, Cop-1 treatment led to anti-inflammatory and neuroprotective responses. Reduced micro- and astrogliosis, and conserved NeuN/MAP-2 levels were observed in virus-affected brain regions in Cop-1-treated mice. These were linked to interleukin-10 and brain-derived neurotrophic factor expression and downregulation of inducible nitric oxide synthase. The data, taken together, demonstrate that Cop-1 can modulate innate immunity and, as such, improve disease outcomes in an animal model of HIVE.

Indexed as

AnimalsApoptosisCells, CulturedCell SurvivalDisease Models, AnimalDose-Response Relationship, DrugEmbryo, MammalianEncephalitis, ViralGene Expression Regulation, ViralGlatiramer AcetateGlial Fibrillary Acidic ProteinHIV InfectionsHumansImmunity, InnateImmunosuppressive AgentsIn Situ Nick-End LabelingGlatiramer AcetateGlial Fibrillary Acidic ProteinImmunosuppressive AgentsPeptides

Identifiers

PMID18046731
PMCPMC2734453
OpenAlexW2070772192

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.