Evidence map›Paper›PMID 26745156›Full record

ArticlePLoS neglected tropical diseases2016

Genetically Determined MBL Deficiency Is Associated with Protection against Chronic Cardiomyopathy in Chagas Disease.

Paola Rosa Luz, Márcia I Miyazaki, Nelson Chiminacio Neto, Marcela C Padeski, Ana Cláudia M Barros, Angelica B W Boldt, Iara J Messias-Reason

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
4.3field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. New insights intoFrontiers in immunology · 2024
    Review
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  6. Case Report: High Mannose-Binding Lectin Serum Determined byThe American journal of tropical medicine and hygiene · 2019
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  7. Article
  8. Article
  9. Article
  10. Review
  11. BALB/c and C57BL/6 Mice Cytokine Responses toFrontiers in microbiology · 2018
    Article
  12. Review
  13. The Complement System: A Prey ofFrontiers in microbiology · 2017
    Review
  14. Article
  15. Review
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

7 authors at 2 institutions in 1 country.

Paola Rosa LuzLaboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Márcia I MiyazakiAmbulatório de Atenção ao Paciente Chagásico-Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Nelson Chiminacio NetoServiço de Ecocardiografia-Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Marcela C PadeskiLaboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Ana Cláudia M BarrosLaboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Angelica B W BoldtLaboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Iara J Messias-ReasonLaboratório de Imunopatologia Molecular-Departamento de Patologia Médica, Hospital de Clínicas, Universidade Federal do Paraná, Curitiba, Brasil.
Hospital de Clínicas Universidade Federal do Paraná · BRUniversidade Federal do Paraná · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chagas disease (CD) is caused by Trypanosoma cruzi, whose sugar moieties are recognized by mannan binding lectin (MBL), a soluble pattern-recognition molecule that activates the lectin pathway of complement. MBL levels and protein activity are affected by polymorphisms in the MBL2 gene. We sequenced the MBL2 promoter and exon 1 in 196 chronic CD patients and 202 controls. The MBL2*C allele, which causes MBL deficiency, was associated with protection against CD (P = 0.007, OR = 0.32). Compared with controls, genotypes with this allele were completely absent in patients with the cardiac form of the disease (P = 0.003). Furthermore, cardiac patients with genotypes causing MBL deficiency presented less heart damage (P = 0.003, OR = 0.23), compared with cardiac patients having the XA haplotype causing low MBL levels, but fully capable of activating complement (P = 0.005, OR = 7.07). Among the patients, those with alleles causing MBL deficiency presented lower levels of cytokines and chemokines possibly implicated in symptom development (IL9, p = 0.013; PDGFB, p = 0.036 and RANTES, p = 0.031). These findings suggest a protective effect of genetically determined MBL deficiency against the development and progression of chronic CD cardiomyopathy.

Indexed as

Disease ResistanceMetabolism, Inborn ErrorsAdultAgedAged, 80 and overChagas CardiomyopathyFemaleHumansMaleMannose-Binding LectinMiddle AgedYoung AdultMannose-Binding LectinMBL2 protein, human

Identifiers

PMID26745156
PMCPMC4706301
OpenAlexW2224491527

What OpenQuestion holds

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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.