Evidence map›Paper›PMID 30995222›Full record

ArticlePLoS neglected tropical diseases2019

Human collectin-11 (COLEC11) and its synergic genetic interaction with MASP2 are associated with the pathophysiology of Chagas Disease.

Thaisa Lucas Sandri, Fabiana Antunes Andrade, Kárita Cláudia Freitas Lidani, Elias Einig, Angelica Beate Winter Boldt, Benjamin Mordmüller, Meral Esen, Iara J Messias-Reason

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

Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
0.8field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
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  5. Review
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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

8 authors at 2 institutions in 2 countries.

Thaisa Lucas SandriInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.ORCID 0000-0001-6039-5241
Fabiana Antunes AndradeLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.
Kárita Cláudia Freitas LidaniLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.
Elias EinigInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.ORCID 0000-0001-7142-1281
Angelica Beate Winter BoldtLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.
Benjamin MordmüllerInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Meral EsenInstitute of Tropical Medicine, University of Tübingen, Tübingen, Germany.
Iara J Messias-ReasonLaboratory of Molecular Immunopathology, Department of Clinical Pathology, Federal University of Paraná, Curitiba, Brazil.
Universidade Federal do Paraná · BRUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chagas Disease (CD) is an anthropozoonosis caused by Trypanosoma cruzi. With complex pathophysiology and variable clinical presentation, CD outcome can be influenced by parasite persistence and the host immune response. Complement activation is one of the primary defense mechanisms against pathogens, which can be initiated via pathogen recognition by pattern recognition molecules (PRMs). Collectin-11 is a multifunctional soluble PRM lectin, widely distributed throughout the body, with important participation in host defense, homeostasis, and embryogenesis. In complex with mannose-binding lectin-associated serine proteases (MASPs), collectin-11 may initiate the activation of complement, playing a role against pathogens, including T. cruzi. In this study, collectin-11 plasma levels and COLEC11 variants in exon 7 were assessed in a Brazilian cohort of 251 patients with chronic CD and 108 healthy controls. Gene-gene interactions between COLEC11 and MASP2 variants were analyzed. Collectin-11 levels were significantly decreased in CD patients compared to controls (p<0.0001). The allele rs7567833G, the genotypes rs7567833AG and rs7567833GG, and the COLEC11*GGC haplotype were related to T. cruzi infection and clinical progression towards symptomatic CD. COLEC11 and MASP2*CD risk genotypes were associated with cardiomyopathy (p = 0.014; OR 9.3, 95% CI 1.2-74) and with the cardiodigestive form of CD (p = 0.005; OR 15.2, 95% CI 1.7-137), suggesting that both loci act synergistically in immune modulation of the disease. The decreased levels of collectin-11 in CD patients may be associated with the disease process. The COLEC11 variant rs7567833G and also the COLEC11 and MASP2*CD risk genotype interaction were associated with the pathophysiology of CD.

Indexed as

Epistasis, GeneticAdultAgedAged, 80 and overBrazilCase-Control StudiesChagas DiseaseCollectinsFemaleGenetic Predisposition to DiseaseHaplotypesHumansMaleMannose-Binding Protein-Associated Serine ProteasesMiddle AgedPolymorphism, Single NucleotideColec11 protein, humanCollectinsMannose-Binding Protein-Associated Serine ProteasesMASP2 protein, human

Identifiers

PMID30995222
PMCPMC6488100
OpenAlexW2938585684

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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.