Evidence map›Paper›PMID 22292031›Full record

ArticlePloS one2012

Plasmid-cured Chlamydia caviae activates TLR2-dependent signaling and retains virulence in the guinea pig model of genital tract infection.

Lauren C Frazer, Toni Darville, Kumar Chandra-Kuntal, Charles W Andrews, Matthew Zurenski, Margaret Mintus, Yasser M AbdelRahman, Robert J Belland, Robin R Ingalls, Catherine M O'Connell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Frontiers in microbiology · 2020
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Chlamydial Plasmid-Dependent Pathogenicity.Trends in microbiology · 2017
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

10 authors at 3 institutions in 2 countries.

Lauren C FrazerDepartment of Pediatrics, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, Pennsylvania, United States of America.
Toni Darville
Kumar Chandra-Kuntal
Charles W Andrews
Matthew Zurenski
Margaret Mintus
Yasser M AbdelRahman
Robert J Belland
Robin R Ingalls
Catherine M O'Connell
Children's Hospital of Pittsburgh · USUniversity of Tennessee Health Science Center · USBoston University · US

Funding

Transcriptional Control of Chlamydial DevelopmentR01AI070693 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BELLAND, ROBERT J · 2008 to 2012
$1.8M
Interaction of Chlamydia with Innate Immune ReceptorsR01AI064749 · NIAID · BOSTON MEDICAL CENTER · PI INGALLS, ROBIN R · 2005 to 2009
$1.5M
TLR2 ligands of chlamydiaeR21AI083657 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI O'CONNELL, CATHERINE MARY · 2009 to 2010
$417k
NIAID NIH HHS R01 AI064749NIAID NIH HHS R01 AI070693NIAID NIH HHS R21 AI083657
6 · The paper itself

Abstract

Loss of the conserved "cryptic" plasmid from C. trachomatis and C. muridarum is pleiotropic, resulting in reduced innate inflammatory activation via TLR2, glycogen accumulation and infectivity. The more genetically distant C. caviae GPIC is a natural pathogen of guinea pigs and induces upper genital tract pathology when inoculated intravaginally, modeling human disease. To examine the contribution of pCpGP1 to C. caviae pathogenesis, a cured derivative of GPIC, strain CC13, was derived and evaluated in vitro and in vivo. Transcriptional profiling of CC13 revealed only partial conservation of previously identified plasmid-responsive chromosomal loci (PRCL) in C. caviae. However, 2-deoxyglucose (2DG) treatment of GPIC and CC13 resulted in reduced transcription of all identified PRCL, including glgA, indicating the presence of a plasmid-independent glucose response in this species. In contrast to plasmid-cured C. muridarum and C. trachomatis, plasmid-cured C. caviae strain CC13 signaled via TLR2 in vitro and elicited cytokine production in vivo similar to wild-type C. caviae. Furthermore, inflammatory pathology induced by infection of guinea pigs with CC13 was similar to that induced by GPIC, although we observed more rapid resolution of CC13 infection in estrogen-treated guinea pigs. These data indicate that either the plasmid is not involved in expression or regulation of virulence in C. caviae or that redundant effectors prevent these phenotypic changes from being observed in C. caviae plasmid-cured strains.

Indexed as

AnimalsCells, CulturedChlamydiaChlamydia InfectionsDisease Models, AnimalEvolution, MolecularFemaleGene DeletionGuinea PigsHEK293 CellsHumansLymphocyte ActivationPlasmidsReproductive Tract InfectionsSignal TransductionToll-Like Receptor 2Toll-Like Receptor 2

Identifiers

PMID22292031
PMCPMC3265510
OpenAlexW1994034391

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.