Evidence map›Paper›PMID 27481250›Full record

ArticleInfection and immunity2016

The Aryl Hydrocarbon Receptor Modulates Production of Cytokines and Reactive Oxygen Species and Development of Myocarditis during Trypanosoma cruzi Infection.

Andréia Barroso, Melisa Gualdrón-López, Lísia Esper, Fátima Brant, Ronan R S Araújo, Matheus B H Carneiro, Thiago V Ávila, Danielle G Souza, Leda Q Vieira, Milene A Rachid and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
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  11. The aryl hydrocarbon receptor and the gut-brain axis.Cellular & molecular immunology · 2021
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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

13 authors at 2 institutions in 2 countries.

Andréia BarrosoProgram in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Melisa Gualdrón-LópezDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Lísia EsperProgram in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Fátima BrantProgram in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Ronan R S AraújoDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Matheus B H CarneiroDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Thiago V ÁvilaDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Danielle G SouzaDepartment of Microbiology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Leda Q VieiraDepartment of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Milene A RachidDepartment of Pathology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Herbert B TanowitzDepartments of Pathology and Medicine, Albert Einstein College of Medicine, Bronx, New York, USA.
Mauro M TeixeiraProgram in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Fabiana S MachadoProgram in Health Sciences: Infectious Diseases and Tropical Medicine, Medical School, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil machadofs@icb.ufmg.br.
Universidade Federal de Minas Gerais · BRAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved in controlling several aspects of immune responses, including the activation and differentiation of specific T cell subsets and antigen-presenting cells, thought to be relevant in the context of experimental Trypanosoma cruzi infection. The relevance of AhR for the outcome of T. cruzi infection is not known and was investigated here. We infected wild-type (WT) mice and AhR knockout (AhR KO) mice with T. cruzi (Y strain) and determined levels of parasitemia, myocardial inflammation and fibrosis, expression of AhR/cytokines/suppressor of cytokine signaling (SOCS) (spleen/heart), and production of nitric oxide (NO), reactive oxygen species (ROS), and peroxynitrite (ONOO(-)) (spleen). AhR expression was increased in the heart of infected WT mice. Infected AhR KO mice displayed significantly reduced parasitemia, inflammation, and fibrosis of the myocardium. This was associated with an anticipated increased immune response characterized by increased levels of inflammatory cytokines and reduced expression of SOCS2 and SOCS3 in the heart. In vitro, AhR deficiency caused impairment in parasite replication and decreased levels of ROS production. In conclusion, AhR influences the development of murine Chagas disease by modulating ROS production and regulating the expression of key physiological regulators of inflammation, SOCS1 to -3, associated with the production of cytokines during experimental T. cruzi infection.

Indexed as

AnimalsChagas CardiomyopathyChagas DiseaseCytokinesDisease Models, AnimalMiceMice, KnockoutMyocarditisNitric OxidePeroxynitrous AcidReactive Oxygen SpeciesReceptors, Aryl HydrocarbonSpleenSuppressor of Cytokine Signaling ProteinsTrypanosoma cruziCytokinesNitric OxidePeroxynitrous AcidReactive Oxygen SpeciesReceptors, Aryl HydrocarbonSuppressor of Cytokine Signaling Proteins

Identifiers

PMID27481250
PMCPMC5038084
OpenAlexW2507039591

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.