Evidence map›Paper›PMID 25227937›Full record

ArticleBritish journal of anaesthesia2015

Macrophage-sensory neuronal interaction in HIV-1 gp120-induced neurotoxicity‡.

P J Moss, W Huang, J Dawes, K Okuse, S B McMahon, A S C Rice

Open access · hybridAbstract read
In one paragraph

Article in British journal of anaesthesia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 24% 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, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  13. Chronic Pain in HIV.Molecular pain
    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

6 authors at 5 institutions in 1 country.

P J MossPain Research Group, Department of Surgery and Cancer, Faculty of Medicine and.
W HuangPain Research Group, Department of Surgery and Cancer, Faculty of Medicine and Current address: Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK w.huang@abdn.ac.uk.
J DawesWolfson Centre for Age Related Disease, King's College London, London, UK Current address: The Nuffield Department of Clinical Neurosciences, Medical Sciences Division, University of Oxford, Oxford, UK.
K OkuseDepartment of Life Sciences, Faculty of Natural Sciences, Imperial College London, London, UK.
S B McMahonWolfson Centre for Age Related Disease, King's College London, London, UK.
A S C RicePain Research Group, Department of Surgery and Cancer, Faculty of Medicine and Pain Medicine, Chelsea and Westminster Hospital NHS Foundation Trust, London, UK.
Chelsea and Westminster Hospital NHS Foundation Trust · GBImperial College London · GBKing's College London · GBUniversity of Aberdeen · GBUniversity of Oxford · GB

Funding

Wellcome Trust 083259
6 · The paper itself

Abstract

backgroundHuman immunodeficiency virus (HIV)-associated sensory neuropathy (SN) is the most frequent neurological complication of HIV disease. Among the probable mechanisms underlying HIV-SN are neurotoxicity induced by the HIV glycoprotein gp120 and antiretroviral therapies (ART). Since HIV-SN prevalence remains high in patients who have not been exposed to toxic ART drugs, here we focused on gp120-mediated mechanisms underlying HIV-SN.

methodsWe hypothesized that a direct gp120-sensory neurone interaction is not the cause of neurite degeneration; rather, an indirect interaction of gp120 with sensory neurones involving macrophages underlies axonal degeneration. Rat dorsal root ganglion (DRG) cultures were used to assess gp120 neurotoxicity. Rat bone marrow-derived macrophage (BMDM) cultures and qPCR array were used to assess gp120-associated gene expression changes.

resultsgp120 induced significant, but latent onset, neurite degeneration until 24 h after application. gp120-neurone interaction occurred within 1 h of application in <10% of DRG neurones, despite neurite degeneration having a global effect. Application of culture media from gp120-exposed BMDMs induced a significant reduction in DRG neurite outgrowth. Furthermore, gp120 significantly increased the expression of 25 cytokine-related genes in primary BMDMs, some of which have been implicated in other painful polyneuropathies. The C-C chemokine receptor type 5 (CCR5) antagonist, maraviroc, concentration-dependently inhibited gp120-induced tumour necrosis factor-α gene expression, indicating that these effects occurred via gp120 activation of CCR5.

conclusionsOur findings highlight macrophages in the pathogenesis of HIV-SN and upstream modulation of macrophage response as a promising therapeutic strategy.

Indexed as

HIV-1AnimalsCell Culture TechniquesCells, CulturedDisease Models, AnimalFemaleGene ExpressionHIV Envelope Protein gp120MacrophagesNerve DegenerationNeurotoxicity SyndromesPeripheral Nervous System DiseasesPolymerase Chain ReactionRatsRats, WistarSensory Receptor CellsHIV Envelope Protein gp120cytokines; HIV envelope protein; macrophages; maraviroc; peripheral nervous system diseasesperipheral neuropathies

Identifiers

PMID25227937
PMCPMC4332570
OpenAlexW2164240213

What OpenQuestion holds

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LicenceCC BY
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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.