The Role of ST2 Receptor in the Regulation of <i>Brucella abortus</i> Oral Infection
Raiany Santos,
Priscila C. Campos,
Marcella Rungue,
Victor Rocha,
David Santos,
Viviani Mendes,
Fabio V. Marinho,
Flaviano Martins,
Mayra F. Ricci,
Diego C. dos Reis,
Geovanni D. Cassali,
José Carlos Alves-Filho,
Angelica T. Vieira,
Sergio C. Oliveira
Affiliations
Raiany Santos
Department of Genetics, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Priscila C. Campos
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Marcella Rungue
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Victor Rocha
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
David Santos
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Viviani Mendes
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Fabio V. Marinho
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Flaviano Martins
Department of Microbiology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Mayra F. Ricci
Department of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Diego C. dos Reis
Department of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Geovanni D. Cassali
Department of General Pathology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
José Carlos Alves-Filho
Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto 14049-900, Brazil
Angelica T. Vieira
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
Sergio C. Oliveira
Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais—Belo Horizonte, Minas Gerais 31270-901, Brazil
The ST2 receptor plays an important role in the gut such as permeability regulation, epithelium regeneration, and promoting intestinal immune modulation. Here, we studied the role of ST2 receptor in a murine model of oral infection with Brucella abortus, its influence on gut homeostasis and control of bacterial replication. Balb/c (wild-type, WT) and ST2 deficient mice (ST2−/−) were infected by oral gavage and the results were obtained at 3 and 14 days post infection (dpi). Our results suggest that ST2−/− are more resistant to B. abortus infection, as a lower bacterial colony-forming unit (CFU) was detected in the livers and spleens of knockout mice, when compared to WT. Additionally, we observed an increase in intestinal permeability in WT-infected mice, compared to ST2−/− animals. Breakage of the intestinal epithelial barrier and bacterial dissemination might be associated with the presence of the ST2 receptor; since, in the knockout mice no change in intestinal permeability was observed after infection. Together with enhanced resistance to infection, ST2−/− produced greater levels of IFN-γ and TNF-α in the small intestine, compared to WT mice. Nevertheless, in the systemic model of infection ST2 plays no role in controlling Brucella replication in vivo. Our results suggest that the ST2 receptor is involved in the invasion process of B. abortus by the mucosa in the oral infection model.
