Evidence map›Paper›PMID 25536401›Full record

ArticleJournal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research2015

Transcriptional Regulation of CXCL5 in HIV-1-Infected Macrophages and Its Functional Consequences on CNS Pathology.

Debjani Guha, Cynthia R Klamar, Todd Reinhart, Velpandi Ayyavoo

Open access · greenAbstract read
In one paragraph

Article in Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Neutrophils and viral-induced neurologic disease.Clinical immunology (Orlando, Fla.) · 2018
    Review
  9. Article
  10. Article
  11. Heart-resident CCR2JCI insight · 2016
    Article
  12. Article
  13. Review
  14. Article
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

4 authors at 1 institution in 1 country.

Debjani GuhaDepartment of Infectious Diseases and Microbiology, Graduate School of Public Health, University of Pittsburgh , Pittsburgh, Pennsylvania.
Cynthia R Klamar
Todd Reinhart
Velpandi Ayyavoo
University of Pittsburgh · US

Funding

University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
Training and Research on Effectiveness of Antiretroviral TherapyD43TW001038 · FIC · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HARRISON, LEE H · 1998 to 2013
$4.7M
HIV-1 Associated Dementia: Concomitant Roles of Vpr and Cellular FactorsR01MH087247 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AYYAVOO, VELPANDI · 2010 to 2014
$1.7M
FIC NIH HHS D43TW001038NCATS NIH HHS UL1 TR000005NIMH NIH HHS R01 MH087247
6 · The paper itself

Abstract

Human immunodeficiency virus-1 (HIV-1)-infected monocytes/macrophages and microglia release increased levels of proinflammatory cytokines and chemokines, including ELR+ (containing glutamic acid-leucine-arginine motif) chemokines. To investigate the role of HIV-1 infection on chemokine regulation, monocyte-derived macrophages (MDMs) from normal donors were infected with HIV-1 and the expression of chemokines and their downstream biological functions were evaluated. Among the tested chemokines, CXCL5 was upregulated significantly both at the mRNA and protein level in the HIV-1-infected MDMs compared with mock-infected cultures. Upregulation of CXCL5 in the HIV-1-infected MDMs is, in part, regulated by increased interleukin-1β (IL-1β) production and phosphorylation of ERK1/2. Functional analyses indicate that HIV-1-induced overexpression of CXCL5 has enhanced the ability to attract neutrophils, as observed by chemotaxis assay. However, exposure of NT2, SH-SY5Y cells, and primary neurons to HIV-1-infected MDM supernatants resulted in cell death that was not rescued by anti-CXCL5 antibody suggesting that CXCL5 does not have direct effect on neuronal death. Together, these results suggest that the increased level of CXCL5 in tissue compartments, including the central nervous system of HIV-1-infected individuals might alter the inflammatory response through the infiltration of neutrophils into tissue compartment, thus causing secondary effects on resident cells.

Indexed as

Gene Expression RegulationTranscription, GeneticCell LineCell SurvivalCentral Nervous System Viral DiseasesChemokine CXCL5ChemokinesGene Expression ProfilingHIV-1HIV InfectionsHumansInflammation MediatorsInterleukin-1betaMacrophagesMAP Kinase Signaling SystemNeuronsChemokine CXCL5ChemokinesInflammation MediatorsInterleukin-1beta

Identifiers

PMID25536401
PMCPMC4426304
OpenAlexW1986015261

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.