Evidence map›Paper›PMID 21697459›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Akt-mediated proinflammatory response of mononuclear phagocytes infected with Burkholderia cenocepacia occurs by a novel GSK3β-dependent, IκB kinase-independent mechanism.

Thomas J Cremer, Prexy Shah, Estelle Cormet-Boyaka, Miguel A Valvano, Jonathan P Butchar, Susheela Tridandapani

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Review
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  7. BioMed research international · 2018
    Article
  8. Article
  9. Low-level arsenic causes chronic inflammation and suppresses expression of phagocytic receptors.Environmental science and pollution research international · 2017
    Article
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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

6 authors at 3 institutions in 2 countries.

Thomas J CremerDepartment of Internal Medicine, The Ohio State University Medical Center, Columbus, OH 43210, USA.
Prexy Shah
Estelle Cormet-Boyaka
Miguel A Valvano
Jonathan P Butchar
Susheela Tridandapani
The Ohio State University · USThe Ohio State University Wexner Medical Center · USWestern University · CA

Funding

Vaccines and Therapies Against BotulismU54AI057153 · NIAID · UNIVERSITY OF CHICAGO · PI MISSIAKAS, DOMINIQUE M. · 2003 to 2013
$87.6M
SHIP-2 influence on macrophage Fc receptor functionR01AI059406 · NIAID · OHIO STATE UNIVERSITY · PI TRIDANDAPANI, SUSHEELA · 2005 to 2009
$1.4M
Interdisciplinary Study of the Microbe-Host InterfaceT32AI065411 · NIAID · OHIO STATE UNIVERSITY · PI SCHLESINGER, LARRY S. · 2007 to 2011
$592k
NIAID NIH HHS 1-T32-AI-065411NIAID NIH HHS 1-U54-AI-057153NIAID NIH HHS R01 AI059406NIAID NIH HHS T32 AI065411NIAID NIH HHS U54 AI057153
6 · The paper itself

Abstract

The environmental bacterium Burkholderia cenocepacia causes opportunistic lung infections in immunocompromised individuals, particularly in patients with cystic fibrosis. Infections in these patients are associated with exacerbated inflammation leading to rapid decay of lung function, and in some cases resulting in cepacia syndrome, which is characterized by a fatal acute necrotizing pneumonia and sepsis. B. cenocepacia can survive intracellularly in macrophages by altering the maturation of the phagosome, but very little is known on macrophage responses to the intracellular infection. In this study, we have examined the role of the PI3K/Akt signaling pathway in B. cenocepacia-infected monocytes and macrophages. We show that PI3K/Akt activity was required for NF-κB activity and the secretion of proinflammatory cytokines during infection with B. cenocepacia. In contrast to previous observations in epithelial cells infected with other Gram-negative bacteria, Akt did not enhance IκB kinase or NF-κB p65 phosphorylation, but rather inhibited GSK3β, a negative regulator of NF-κB transcriptional activity. This novel mechanism of modulation of NF-κB activity may provide a unique therapeutic target for controlling excessive inflammation upon B. cenocepacia infection.

Indexed as

AnimalsBurkholderia cenocepaciaBurkholderia InfectionsDown-RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansI-kappa B KinaseInflammation MediatorsMacrophagesMiceMonocytesPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, mouseI-kappa B KinaseInflammation MediatorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTranscription Factor RelA

Identifiers

PMID21697459
PMCPMC3131456
OpenAlexW2114733747

What OpenQuestion holds

Textmetadata
LicenceTDM
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.