Evidence map›Paper›PMID 25295030›Full record

ArticleFrontiers in microbiology2014

Gene polymorphisms in pattern recognition receptors and susceptibility to idiopathic recurrent vulvovaginal candidiasis.

Diana C Rosentul, Corine E Delsing, Martin Jaeger, Theo S Plantinga, Marije Oosting, Irene Costantini, Hanka Venselaar, Leo A B Joosten, Jos W M van der Meer, Bertrand Dupont and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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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

13 authors at 4 institutions in 3 countries.

Diana C RosentulDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Corine E DelsingDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Martin JaegerDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Theo S PlantingaDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Marije OostingDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Irene CostantiniDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Hanka VenselaarCentre for Molecular and Biomolecular Informatics, Nijmegen Center for Molecular Life Science, Radboud University Medical Center Nijmegen, Netherlands.
Leo A B JoostenDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Jos W M van der MeerDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Bertrand DupontHôpital Necker-Enfants Malades Paris, France.
Bart-Jan KullbergDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Jack D SobelDepartment of Medicine, School of Medicine, Wayne State University Detroit, MI, USA ; Division of Infectious Diseases, Harper University Hospital Detroit, MI, USA.
Mihai G NeteaDepartment of Internal Medicine, Radboud University Medical Center Nijmegen, Netherlands ; Nijmegen Institute for Infection, Inflammation and Immunity (N4i), Radboud University Medical Center Nijmegen, Netherlands.
Radboud University Nijmegen · NLRadboud University Medical Center · NLHarper University Hospital · USHôpital Necker-Enfants Malades · FR

Funding

European Research Council 310372
6 · The paper itself

Abstract

objectiveApproximately 5% of women suffer from recurrent vulvovaginal candidiasis (RVVC). It has been hypothesized that genetic factors play an important role in the susceptibility to RVVC. The aim of this study was to assess the effect of genetic variants of genes encoding for pattern recognition receptors (PRRs) on susceptibility to RVVC. STUDY

designFor the study, 119 RVVC patients and 263 healthy controls were recruited. Prevalence of polymorphisms in five PRRs involved in recognition of Candida were investigated in patients and controls. In silico and functional studies were performed to assess their functional effects.

resultsSingle nucleotide polymorphisms (SNPs) in TLR1, TLR4, CLEC7A, and CARD9 did not affect the susceptibility to RVVC. In contrast, a non-synonymous polymorphism in TLR2 (rs5743704, Pro631His) increased the susceptibility to RVVC almost 3-fold. Furthermore, the TLR2 rs5743704 SNP had deleterious effects on protein function as assessed by in silico analysis, and in vitro functional assays suggested that it reduces production of IL-17 and IFNγ upon stimulation of peripheral blood mononuclear cells with Candida albicans. No effects were observed on serum mannose-binding lectin concentrations. CONDENSATION: This study demonstrates the association of susceptibility to RVVC with genetic variation in TLR2, most likely caused by decreased induction of mucosal antifungal host defense.

conclusionGenetic variation in TLR2 may significantly enhance susceptibility to RVVC by modulating host defense mechanisms against Candida. Additional studies are warranted to assess systematically the role of host genetic variation for susceptibility to RVVC.

Indexed as

cytokinesgenetic variationpattern recognition receptorsRVVC

Identifiers

PMID25295030
PMCPMC4172055
OpenAlexW2036655441

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.