Evidence map›Paper›PMID 29319809›Full record

ArticleJournal of neuropathology and experimental neurology2018

Increased Microglial CSF1R Expression in the SIV/Macaque Model of HIV CNS Disease.

Audrey C Knight, Samuel A Brill, Suzanne E Queen, Patrick M Tarwater, Joseph L Mankowski

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Article
  8. Article
  9. The reservoir of latent HIV.Frontiers in cellular and infection microbiology · 2022
    Review
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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

5 authors at 3 institutions in 1 country.

Audrey C KnightDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Samuel A BrillDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Suzanne E QueenDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Patrick M TarwaterDepartment of Biostatistics, UTHealth School of Public Health, El Paso, Texas.
Joseph L MankowskiDepartment of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Johns Hopkins Medicine · USJohns Hopkins University · USUniversity of Texas Health Science Center at Dallas · US

Funding

Vaccine Response and Immunotherapeutics SWGP30AI094189 · NIAID · JOHNS HOPKINS UNIVERSITY · PI Richard E. Chaisson · 2012 to 2026
$67.0M
Viral Testing CoreU42OD013117 · OD · JOHNS HOPKINS UNIVERSITY · PI Lydia Hopper · 2017 to 2026
$10.9M
Dual-Degree Medical Scientist Training Program for VeterinariansT32GM136628 · NIGMS · COLORADO STATE UNIVERSITY · PI ANNE C AVERY, Daniel Patrick Regan · 2020 to 2026
$1.9M
NIAID NIH HHS P30 AI094189NIGMS NIH HHS T32 GM136628NIH HHS U42 OD013117
6 · The paper itself

Abstract

Chronic microglial activation and associated neuroinflammation are key factors in neurodegenerative diseases including HIV-associated neurocognitive disorders. Colony stimulating factor 1 receptor (CSF1R)-mediated signaling is constitutive in cells of the myeloid lineage, including microglia, promoting cell survival, proliferation, and differentiation. In amyotrophic lateral sclerosis and Alzheimers disease, CSF1R is upregulated. Inhibiting CSF1R signaling in animal models of these diseases improved disease outcomes. In our studies, CNS expression of the CSF1R ligand, colony-stimulating factor 1 (CSF1) was significantly increased in a SIV/macaque model of HIV CNS disease. Using a Nanostring nCounter immune panel, we found CSF1 overexpression was strongly correlated with upregulation of microglial genes involved in antiviral and oxidative stress responses. Using in situ hybridization, we found that CSF1R mRNA was only present in Iba-1 positive microglia. By ELISA and immunostaining with digital image analysis, SIV-infected macaques had significantly higher CSF1R levels in frontal cortex than uninfected macaques (p = 0.018 and p = 0.02, respectively). SIV-infected macaques treated with suppressive ART also had persistently elevated CSF1R similar to untreated SIV-infected macaques. Coordinate upregulation of CSF1 and CSF1R expression implicates this signaling pathway in progressive HIV CNS disease.

Indexed as

Central Nervous System DiseasesAnimalsBrainDisease Models, AnimalGene Expression Regulation, ViralInterleukinsMacaca nemestrinaMaleMicrogliaOxidative StressReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRNA, MessengerSimian Acquired Immunodeficiency SyndromeInterleukinsReceptors, Granulocyte-Macrophage Colony-Stimulating FactorRNA, MessengerColony stimulating factor 1 (CSF1)Colony stimulating factor 1 receptor (CSF1R)Human immunodeficiency virus (HIV)MacaqueMicrogliaNeurodegenerationSimian immunodeficiency virus (SIV)

Identifiers

PMID29319809
PMCPMC6251515
OpenAlexW2783469156

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.