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3150-12-31
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ENTEROPATHOGENIC ESCHERICHIA COLI MODULATES THE VIRULENCE AND PATHOGENICITY OF ENTAMOEBA DISPAR.
Amoebic liver abscess
Enteropathogenic Escherichia coli
Galactose/N-acetyl-D-galactosamine-binding lectin
Cysteine proteinase 2
Amoebapores
Author
Silva, Cezar Augusto Vilela da
Santos, Carlos Eduardo Costa dos
Cortezzi, Mariana Fernandes de Paula
Moura, César da Silva Santana
Cruz, Ruth Elizabeth
Lopes, Camila de Almeida
Costa, Karen
Souza, Lucas Teixeira de
Silva, Patrícia Costa Lima da
Neumann, Elisabeth
Nunes, Álvaro Cantini
Gomes, Maria Aparecida
Oliveira, Fabrício Marcus Silva
Caliari, Marcelo Vidigal
Santos, Carlos Eduardo Costa dos
Cortezzi, Mariana Fernandes de Paula
Moura, César da Silva Santana
Cruz, Ruth Elizabeth
Lopes, Camila de Almeida
Costa, Karen
Souza, Lucas Teixeira de
Silva, Patrícia Costa Lima da
Neumann, Elisabeth
Nunes, Álvaro Cantini
Gomes, Maria Aparecida
Oliveira, Fabrício Marcus Silva
Caliari, Marcelo Vidigal
Affilliation
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Cellular and Molecular Immunology Group. Rene Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Microbiology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Genetics, Ecology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Department of Parasitology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Cellular and Molecular Immunology Group. Rene Rachou Institute. Oswaldo Cruz Foundation. Belo Horizonte, MG, Brazil
Department of General Pathology. Institute of Biological Sciences. Federal University of Minas Gerais. Belo Horizonte, MG, Brazil.
Abstract
Amoebiasis is a disease caused by Entamoeba histolytica, affecting the large intestine of humans and occasionally leading to extra-intestinal lesions. Entamoeba dispar is another amoeba species considered commensal, although it has been identified in patients presenting with dysenteric and nondysenteric colitis, as well as amoebic liver abscess. Amoebic virulence factors are essential for the invasion and development of lesions. There is evidence showing that the association of enterobacteria with trophozoites contributes to increased gene expression of amoebic virulence factors. Enteropathogenic Escherichia coli is an important bacterium causing diarrhea, with high incidence rates in the world population, allowing it to interact with Entamoeba sp. in the same host. In this context, this study aims to evaluate the influence of enteropathogenic Escherichia coli on ACFN and ADO Entamoeba dispar strains by quantifying the gene expression of virulence factors, including galactose/N-acetyl-D-galactosamine-binding lectin, cysteine proteinase 2, and amoebapores A and C. Additionally, the study assesses the progression and morphological aspect of amoebic liver abscess and the profile of inflammatory cells. Our results demonstrated that the interaction between EPEC and ACFN Entamoeba dispar strains was able to increase the gene expression of virulence factors, as well as the lesion area and the activity of the inflammatory infiltrate. However, the association with the ADO strain did not influence the gene expression of virulence factors. Together, our findings indicate that the interaction between EPEC, ACFN, and ADO Entamoeba dispar strains resulted in differences in vitro and in vivo gene expression of Gal/GalNAc-binding lectin and CP2, in enzymatic activities of MPO, NAG, and EPO, and consequently, in the ability to cause lesions.
Keywords
Entamoeba disparAmoebic liver abscess
Enteropathogenic Escherichia coli
Galactose/N-acetyl-D-galactosamine-binding lectin
Cysteine proteinase 2
Amoebapores
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