Evidence map›Paper›PMID 18985732›Full record

ArticleGlia2009

Proinflammatory cytokines and HIV-1 synergistically enhance CXCL10 expression in human astrocytes.

Rachel Williams, Navneet K Dhillon, Sonia T Hegde, Honghong Yao, Fuwang Peng, Shannon Callen, Yahia Chebloune, Randall L Davis, Shilpa J Buch

Abstract read
In one paragraph

Article in Glia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.7field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 75 citations in OpenAlex.

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  18. [Advances of immunological pathogenesis research in HIV related neurocognitive disorder].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016
    Article
  19. 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

9 authors at 3 institutions in 1 country.

Rachel WilliamsDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160, USA.
Navneet K Dhillon
Sonia T Hegde
Honghong Yao
Fuwang Peng
Shannon Callen
Yahia Chebloune
Randall L Davis
Shilpa J Buch
University of Kansas · USUniversity of Kansas Medical Center · USOklahoma State University Oklahoma City · US

Funding

Morphine and the Neuropathogenesis of SIV in MacaquesR01DA024442 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J. · 2007 to 2011
$2.8M
Mechanism and Therapy of SHIV Encephalitis in MacaquesR01MH068212 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J. · 2003 to 2012
$2.7M
HIV-Encephalitis and Cocaine Abuse: Mechanism of Synergy and TherapyR01DA020392 · NIDA · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BUCH, SHILPA J. · 2006 to 2010
$1.4M
Ethanol Effects on Human Astroglial Chemokine ExpressionR21AA014955 · NIAAA · OSU CENTER FOR HEALTH SCIENCES · PI DAVIS, RANDALL L · 2006 to 2007
$337k
HIV-Encephalitis: Mechanisms for CXCL 10 Induction in AstrocytesF31NS062665 · NINDS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI WILLIAMS, RACHEL · 2008 to 2009
$32k
NIAAA NIH HHS AA014955NIAAA NIH HHS R21 AA014955NIDA NIH HHS DA020392NIDA NIH HHS DA024442NIDA NIH HHS R01 DA020392NIDA NIH HHS R01 DA024442NIMH NIH HHS MH068212NIMH NIH HHS R01 MH068212NINDS NIH HHS F31 NS062665NINDS NIH HHS F31NS062665
6 · The paper itself

Abstract

HIV encephalitis (HIVE), the pathologic correlate of HIV-associated dementia (HAD) is characterized by astrogliosis, cytokine/chemokine dysregulation, and neuronal degeneration. Increasing evidence suggests that inflammation is actively involved in the pathogenesis of HAD. In fact, the severity of HAD/HIVE correlates more closely with the presence of activated glial cells than with the presence and amount of HIV-infected cells in the brain. Astrocytes, the most numerous cell type within the brain, provide an important reservoir for the generation of inflammatory mediators, including interferon-gamma inducible peptide-10 (CXCL10), a neurotoxin and a chemoattractant, implicated in the pathophysiology of HAD. Additionally, the proinflammatory cytokines, IFN-gamma and TNF-alpha, are also markedly increased in CNS tissues during HIV-1 infection. In this study, we hypothesized that the interplay of host cytokines and HIV-1 could lead to enhanced expression of the toxic chemokine, CXCL10. Our findings demonstrate a synergistic induction of CXCL10 mRNA and protein in human astrocytes exposed to HIV-1 and the proinflammatory cytokines. Signaling molecules, including JAK, STATs, MAPK (via activation of Erk1/2, AKT, and p38), and NF-kappaB were identified as instrumental in the synergistic induction of CXCL10. Understanding the mechanisms involved in HIV-1 and cytokine-mediated up-regulation of CXCL10 could aid in the development of therapeutic modalities for HAD.

Indexed as

AstrocytesBlotting, WesternCell LineChemokine CXCL10CytokinesEnzyme-Linked Immunosorbent AssayGene ExpressionHIV-1HumansImmunohistochemistryInterferon-gammaNF-kappa BPolymerase Chain ReactionRNA, MessengerSignal TransductionTumor Necrosis Factor-alphaChemokine CXCL10CXCL10 protein, humanCytokinesInterferon-gammaNF-kappa BRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID18985732
PMCPMC2667210
OpenAlexW2096482886

What OpenQuestion holds

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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.