Evidence map›Paper›PMID 18354226›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

The synthetic peroxisome proliferator-activated receptor-gamma agonist ciglitazone attenuates neuroinflammation and accelerates encapsulation in bacterial brain abscesses.

Tammy Kielian, Mohsin Md Syed, Shuliang Liu, Nirmal K Phulwani, Napoleon Phillips, Gail Wagoner, Paul D Drew, Nilufer Esen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  5. Review
  6. Article
  7. PPARPPAR research · 2016
    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

8 authors at 1 institution in 1 country.

Tammy KielianDepartment of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. KielianTammyL@uams.edu
Mohsin Md Syed
Shuliang Liu
Nirmal K Phulwani
Napoleon Phillips
Gail Wagoner
Paul D Drew
Nilufer Esen
University of Arkansas for Medical Sciences · US

Funding

VIRULENCE MECHANISMS IN ESCHERICHIA COLIP20RR016460 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI HENSLEY, LORI · 2001 to 2011
$33.1M
THE PATHOGENESIS OF BRAIN ABSCESSR01NS040730 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI KIELIAN, TAMMY L · 2001 to 2013
$3.4M
NEUROSCIENCE RESEARCH CENTER CORE FACILITY AT UAMSP30NS047546 · NINDS · UNIV OF ARKANSAS FOR MED SCIS · PI ZHANG, JUN-MING · 2004 to 2008
$3.1M
ZEISS LSM 510 CONFOCAL MICROSCOPE SYSTEM: CELL BIOLOGYS10RR019395 · NCRR · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI KURTEN, RICHARD C · 2005 to 2005
$339k
MEDICAL INFORMATICS NETWORK-A DISTRIBUTED COMPUTING FACIS10RR006460 · NCRR · UNIVERSITY OF MARYLAND BALTIMORE · PI DE CLARIS, NICHOLAS · 1991 to 1991
–
NCRR NIH HHS P20 RR016460NCRR NIH HHS P20 RR 6460NCRR NIH HHS S10 RR019395NCRR NIH HHS S10 RR 19395NINDS NIH HHS 2 R01 NS 40730NINDS NIH HHS P30 NS 047546NINDS NIH HHS P30 NS047546NINDS NIH HHS R01 NS040730
6 · The paper itself

Abstract

Brain abscesses result from a pyogenic parenchymal infection commonly initiated by Gram-positive bacteria such as Staphylococcus aureus. Although the host immune response elicited following infection is essential for effective bacterial containment, this response also contributes to the significant loss of brain parenchyma by necrosis that may be reduced by modulating the inflammatory response. Ciglitazone, a PPAR-gamma agonist with anti-inflammatory properties, was evaluated for its ability to influence the course of brain abscess development when treatment was initiated 3 days following infection. Interestingly, abscess-associated bacterial burdens were significantly lower following ciglitazone administration, which could be explained, in part, by the finding that ciglitazone enhanced S. aureus phagocytosis by microglia. In addition, ciglitazone attenuated the expression of select inflammatory mediators during brain abscess development including inducible NO synthase, TNF-alpha, IL-1beta, CXCL2, and CCL3. Unexpectedly, ciglitazone also accelerated brain abscess encapsulation, which was typified by the heightened expression of fibronectin and alpha-smooth muscle actin-positive myofibroblasts. Collectively, through its ability to attenuate excessive inflammation and accelerate abscess encapsulation, ciglitazone may effectively sequester brain abscesses and limit bacterial dissemination.

Indexed as

AnimalsBrain AbscessCell WallFibronectinsInflammationLigandsMacrophagesMiceMice, Inbred C57BLMicrobial ViabilityMicrogliaNitric Oxide Synthase Type IIPhagocytosisPPAR gammaProteoglycansSensitivity and SpecificityciglitazoneFibronectinsLigandsNitric Oxide Synthase Type IIPPAR gammaProteoglycansThiazolidinediones

Identifiers

PMID18354226
PMCPMC2396461
OpenAlexW1550500774

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.