Evidence map›Paper›PMID 28241035›Full record

ArticlePLoS neglected tropical diseases2017

Association of a new FCN3 haplotype with high ficolin-3 levels in leprosy.

Fabiana Antunes Andrade, Marcia Holsbach Beltrame, Valéria Bumiller Bini, Letícia Boslooper Gonçalves, Angelica Beate Winter Boldt, Iara Jose de Messias-Reason

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

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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 1 institution in 1 country.

Fabiana Antunes AndradeLaboratory of Molecular Immunopathology, Department of Clinical Pathology, HC/UFPR, Curitiba, PR, Brazil.ORCID 0000-0003-4116-2324
Marcia Holsbach BeltrameLaboratory of Molecular Immunopathology, Department of Clinical Pathology, HC/UFPR, Curitiba, PR, Brazil.
Valéria Bumiller BiniLaboratory of Human Molecular Genetics, Department of Genetics, UFPR, Curitiba, PR, Brazil.
Letícia Boslooper GonçalvesLaboratory of Molecular Immunopathology, Department of Clinical Pathology, HC/UFPR, Curitiba, PR, Brazil.
Angelica Beate Winter BoldtLaboratory of Molecular Immunopathology, Department of Clinical Pathology, HC/UFPR, Curitiba, PR, Brazil.
Iara Jose de Messias-ReasonLaboratory of Molecular Immunopathology, Department of Clinical Pathology, HC/UFPR, Curitiba, PR, Brazil.
Universidade Federal do Paraná · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leprosy is a chronic inflammatory disease caused by Mycobacterium leprae that mainly affects the skin and peripheral nervous system, leading to a high disability rate and social stigma. Previous studies have shown a contribution of genes encoding products of the lectin pathway of complement in the modulation of the susceptibility to leprosy; however, the ficolin-3/FCN3 gene impact on leprosy is currently unknown. The aim of the present study was to investigate if FCN3 polymorphisms (rs532781899: g.1637delC, rs28362807: g.3524_3532insTATTTGGCC and rs4494157: g.4473C>A) and ficolin-3 serum levels play a role in the susceptibility to leprosy. We genotyped up to 190 leprosy patients (being 114 (60%) lepromatous), and up to 245 controls with sequence-specific PCR. We also measured protein levels using ELISA in 61 leprosy and 73 controls. FCN3 polymorphisms were not associated with disease, but ficolin-3 levels were higher in patients with FCN3 *2B1 (CinsA) haplotype (p = 0.032). Median concentration of ficolin-3 was higher in leprosy per se (26034 ng/mL, p = 0.005) and lepromatous patients (28295 ng/mL, p = 0.016) than controls (18231 ng/mL). In addition, high ficolin-3 levels (>33362 ng/mL) were more common in leprosy per se (34.4%) and in lepromatous patients (35.5%) than controls (19.2%; p = 0.045 and p = 0.047, respectively). Our results lead us to suggest that polymorphisms in the FCN3 gene cooperate to increase ficolin-3 concentration and that it might contribute to leprosy susceptibility by favoring M. leprae infection.

Indexed as

Genetic Predisposition to DiseaseHaplotypesAdolescentAdultAgedAged, 80 and overEnzyme-Linked Immunosorbent AssayFemaleGlycoproteinsHumansLectinsLeprosyMaleMiddle AgedPolymerase Chain ReactionPolymorphism, Single NucleotideFCN3 protein, humanGlycoproteinsLectins

Identifiers

PMID28241035
PMCPMC5344521
OpenAlexW2594623851

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.