Evidence map›Paper›PMID 15039360›Full record

ArticleInfection and immunity2004

Pathology affects different organs in two mouse strains chronically infected by a Trypanosoma cruzi clone: a model for genetic studies of Chagas' disease.

Claudio R F Marinho, Daniella Z Bucci, Maria Lúcia Z Dagli, Karina R B Bastos, Marcos G Grisotto, Luiz R Sardinha, Cristiane R G M Baptista, Carlos Penha Gonçalves, Maria Regina D'Império Lima, José M Alvarez

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Dynamics and functional heterogeneity of FOXP3+ regulatory T cells in Trypanosoma cruzi infection: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Pooled it
  2. Frontiers in immunology · 2024
    Article
  3. Insights from the use of erythropoietin in experimental Chagas disease.International journal for parasitology. Drugs and drug resistance · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Chagas disease: still many unsolved issues.Mediators of inflammation · 2014
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. ECG detection of murine chagasic cardiomyopathy.The Journal of parasitology · 2010
    Article
  19. Article
  20. 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

10 authors at 2 institutions in 2 countries.

Claudio R F MarinhoDepartment of Immunology, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, São Paulo, Brazil. marinho@usp.br
Daniella Z Bucci
Maria Lúcia Z Dagli
Karina R B Bastos
Marcos G Grisotto
Luiz R Sardinha
Cristiane R G M Baptista
Carlos Penha Gonçalves
Maria Regina D'Império Lima
José M Alvarez
Instituto Gulbenkian de Ciência · PTUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chagas' disease is a chronic infection caused by Trypanosoma cruzi and represents an important public health burden in Latin America. Frequently the disease evolves undetectable for decades, while in a significant fraction of the affected individuals it culminates in death by heart failure. Here, we describe a novel murine model of the chronic infection with T. cruzi using a stable clone isolated from a human patient (Sylvio X10/4). The infection in the C3H/HePAS mouse strain progresses chronically and is mainly characterized by intense cardiac inflammatory lesions that recapitulate the chronic cardiac pathology observed in the human disease. Moderate striated muscle lesions are also present in C3H/HePAS mice. Viable parasites are detected and recovered from the chronic heart lesions of C3H/HePAS mice, supporting the current notion that development of heart pathology in Chagas' disease is related to parasite persistence in the inflamed tissue. By contrast, in infected A/J mice, chronic inflammatory lesions are targeted to the liver and the skeletal muscle, while pathology and parasites are undetectable in the heart. The phenotypic analysis of F(1) (A/J x C3H/HePAS) and F(2) (A/J x C3H/HePAS) mice suggests that the genetic predisposition to develop the inflammatory lesions caused by T. cruzi (Sylvio X10/4 clone) is heterogeneous because the heart and liver pathology segregate in the F(2) generation. These findings raise the hypothesis that the pathology heterogeneity observed in humans with Chagas' disease (absence and presence of cardiac or digestive chronic lesions) may be attributable to host genetic factors.

Indexed as

Genetic Predisposition to DiseaseAnimalsChagas CardiomyopathyChagas DiseaseChronic DiseaseHeartHumansLiverMiceMice, Inbred AMice, Inbred C3HMice, Inbred StrainsMuscle, SkeletalMyocardiumTrypanosoma cruzi

Identifiers

PMID15039360
PMCPMC375186
OpenAlexW2099520711

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.