Evidence map›Paper›PMID 32240160›Full record

ArticlePLoS neglected tropical diseases2020

Adding MASP1 to the lectin pathway-Leprosy association puzzle: Hints from gene polymorphisms and protein levels.

Hellen Weinschutz Mendes, Angelica Beate Winter Boldt, Ewalda von Rosen Seeling Stahlke, Jens Christian Jensenius, Steffen Thiel, Iara J Taborda Messias-Reason

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PLoS neglected tropical diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Association of Polymorphisms ofInternational journal of molecular sciences · 2020
    Review
  5. Article
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 3 institutions in 2 countries.

Hellen Weinschutz MendesLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil.ORCID 0000-0002-4282-6498
Angelica Beate Winter BoldtLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil.
Ewalda von Rosen Seeling StahlkeHealth State Department of Paraná, Curitiba, Brazil.
Jens Christian JenseniusDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Steffen ThielDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Iara J Taborda Messias-ReasonLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Clinical Hospital, Federal University of Paraná, Curitiba, Brazil.
Hospital de Clínicas Universidade Federal do Paraná · BRAarhus University · DKUniversidade Estadual do Paraná · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDeposition of complement factors on Mycobacterium leprae may enhance phagocytosis. Such deposition may occur through the lectin pathway of complement. Three proteins of the lectin pathway are produced from the gene MASP1: Mannan-binding lectin-associated serine protease 1 (MASP-1) and MASP-3 and mannan-binding lectin-associated protein of 44 kDa (MAp44). Despite their obvious importance, the roles played by these proteins have never been investigated in leprosy disease. METHODOLOGY: We haplotyped five MASP1 polymorphisms by multiplex sequence-specific PCR (intronic rs7609662*G>A and rs13064994*C>T, exon 12 3'-untranslated rs72549262*C>G, rs1109452*C>T and rs850314*G>A) and measured MASP-1, MASP-3 and MAp44 serum levels in 196 leprosy patients (60%, lepromatous) and 193 controls. PRINCIPAL

findingsLower MASP-3 and MAp44 levels were observed in patients, compared with controls (P = 0.0002 and P<0.0001, respectively) and in lepromatous, compared with non-lepromatous patients (P = 0.008 and P = 0.002, respectively). Higher MASP-3 levels were present in controls carrying variants/haplotypes associated with leprosy resistance (rs13064994*T, rs1109452_rs850314*CG within GT_CCG and rs850314*A: OR = 0.5-0.6, Pcorr = 0.01-0.04). Controls with rs1109452*T, included in susceptibility haplotypes (GT_GTG/GT_CTG: OR = 2.0, Pcorr = 0.03), had higher MASP-1 and lower MASP-3 levels (P≤0.009). Those with GC_CCG, presented increasing susceptibility (OR = 1.7, Pcorr = 0.006) and higher MAp44 levels (P = 0.015). MASP-3 expression decreased in patients, compared with controls carrying rs1109452_rs850314*CA or CG (P≤0.02), which may rely on exon 12 CpG methylation and/or miR-2861/miR-3181 mRNA binding.

conclusionPolymorphisms regulating MASP-3/MAp44 availability in serum modulate leprosy susceptibility, underlining the importance of lectin pathway regulation against pathogens that exploit phagocytosis to parasitize host macrophages.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdolescentAdultAgedAged, 80 and overCase-Control StudiesCross-Sectional StudiesFemaleHaplotypesHumansLeprosyMaleMannose-Binding Protein-Associated Serine ProteasesMiddle AgedMycobacterium lepraeMannose-Binding Protein-Associated Serine ProteasesMASP1 protein, human

Identifiers

PMID32240160
PMCPMC7162614
OpenAlexW3014653947

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.