Evidence map›Paper›PMID 27294852›Full record

ArticleVirulence2017

Dectin-1 is required for miR155 upregulation in murine macrophages in response to Candida albicans.

Daniel Paiva Agustinho, Marco Antônio de Oliveira, Aldo Henrique Tavares, Lorena Derengowski, Valentina Stolz, Fernanda Guilhelmelli, Márcia Renata Mortari, Karl Kuchler, Ildinete Silva-Pereira

Open access · goldAbstract read
In one paragraph

Article in Virulence, 2017. 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
0.9field-weighted citation impact, top 26% 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, 20 citations in OpenAlex.

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  11. UpregulatedAnnals of translational medicine · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Daniel Paiva Agustinhoa Departamento de Biologia Celular , Laboratório de Biologia Molecular, Universidade de Brasília , Brasília , DF , Brasil.
Marco Antônio de Oliveiraa Departamento de Biologia Celular , Laboratório de Biologia Molecular, Universidade de Brasília , Brasília , DF , Brasil.
Aldo Henrique Tavaresb Departamento de Biologia Celular , Laboratório de Imunologia Aplicada, Instituto de Biologia, Universidade de Brasília , Brasília , DF , Brasil.
Lorena Derengowskia Departamento de Biologia Celular , Laboratório de Biologia Molecular, Universidade de Brasília , Brasília , DF , Brasil.
Valentina Stolzc Department of Molecular Genetics , Max F. Perutz Laboratories, Medical University of Vienna , Vienna , Austria.
Fernanda Guilhelmellia Departamento de Biologia Celular , Laboratório de Biologia Molecular, Universidade de Brasília , Brasília , DF , Brasil.
Márcia Renata Mortarid Departamento de Ciências Fisiológicas , Laboratório de Neurofarmacologia, Universidade de Brasília , Brasília , DF , Brasil.
Karl Kuchlerc Department of Molecular Genetics , Max F. Perutz Laboratories, Medical University of Vienna , Vienna , Austria.
Ildinete Silva-Pereiraa Departamento de Biologia Celular , Laboratório de Biologia Molecular, Universidade de Brasília , Brasília , DF , Brasil.
Universidade de Brasília · BRMax Perutz Labs · ATMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The commensal fungal pathogen Candida albicans is a leading cause of lethal systemic infections in immunocompromised patients. One of the main mechanisms of host immune evasion and virulence by this pathogen is the switch from yeast form to hyphal growth morphologies. Micro RNAs (miRNAs), a small regulatory non-coding RNA, has been identified as an important part of the immune response to a wide variety of pathogens. In general, miRNAs act by modulating the intensity of inflammatory responses. miRNAs act by base-paring binding to specific sequences of target mRNAs, generally causing their silencing through mRNA degradation or translational repression. To study the impact of C. albicans cell morphology upon host miRNA expression, we investigated the differential modulation of 9 different immune response-related miRNAs in primary murine bone marrow-derived macrophages (BMDMs) exposed to either yeasts or hyphal forms of Candida albicans. Here, we show that the different growth morphologies induce distinct miRNA expression patterns in BMDMs. Interestingly, our data suggest that the C-Type lectin receptor Dectin-1 is a major PRR that orchestrates miR155 upregulation in a Syk-dependent manner. Our results suggest that PRR-mediating signaling events are key drivers of miRNA-mediated gene regulation during fungal pathogenesis.

Indexed as

AnimalsCandida albicansDectin-1Gene Expression Regulation, FungalHyphaeImmune EvasionLectins, C-TypeMacrophagesMiceMicroRNAsReceptors, Pattern RecognitionSignal TransductionSyk KinaseTranscriptional ActivationUp-RegulationDectin-1Lectins, C-TypeMicroRNAsMirn155 microRNA, mouseReceptors, Pattern RecognitionSyk KinaseCandida albicansimmune responsemacrophagesmiR155miRNA

Identifiers

PMID27294852
PMCPMC5963198
OpenAlexW2421966767

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.