Nature Communications (Apr 2018)
Canonical PI3Kγ signaling in myeloid cells restricts Trypanosoma cruzi infection and dampens chagasic myocarditis
- Maria C. Silva,
- Marcela Davoli-Ferreira,
- Tiago S. Medina,
- Renata Sesti-Costa,
- Grace K. Silva,
- Carla D. Lopes,
- Lucas E. Cardozo,
- Fábio N. Gava,
- Konstantina Lyroni,
- Fabrício C. Dias,
- Amanda F. Frade,
- Monique Baron,
- Helder I. Nakaya,
- Florêncio Figueiredo,
- José C. Alves-Filho,
- Fernando Q. Cunha,
- Christos Tsatsanis,
- Christophe Chevillard,
- Edecio Cunha-Neto,
- Emilio Hirsch,
- João S. Silva,
- Thiago M. Cunha
Affiliations
- Maria C. Silva
- Department of Pharmacology, Ribeirão Preto Medical School, University of Sao Paulo
- Marcela Davoli-Ferreira
- Department of Pharmacology, Ribeirão Preto Medical School, University of Sao Paulo
- Tiago S. Medina
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Renata Sesti-Costa
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Grace K. Silva
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Carla D. Lopes
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Lucas E. Cardozo
- Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo
- Fábio N. Gava
- Department of Physiology, Ribeirão Preto Medical School, University of Sao Paulo
- Konstantina Lyroni
- Laboratory of Clinical Chemistry, School of Medicine, University of Crete
- Fabrício C. Dias
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Amanda F. Frade
- Laboratory of Immunology, Heart Institute (InCor), School of Medicine, University of São Paulo
- Monique Baron
- Laboratory of Immunology, Heart Institute (InCor), School of Medicine, University of São Paulo
- Helder I. Nakaya
- Department of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo
- Florêncio Figueiredo
- Laboratory of Pathology, School of Medicine, University of Brasilia, Campus Universitário Darcy Ribeiro
- José C. Alves-Filho
- Department of Pharmacology, Ribeirão Preto Medical School, University of Sao Paulo
- Fernando Q. Cunha
- Department of Pharmacology, Ribeirão Preto Medical School, University of Sao Paulo
- Christos Tsatsanis
- Laboratory of Clinical Chemistry, School of Medicine, University of Crete
- Christophe Chevillard
- TAGC/INSERM U1090, Aix Marseille Université AMU, Parc Scientifique de Luminy case 928
- Edecio Cunha-Neto
- Laboratory of Immunology, Heart Institute (InCor), School of Medicine, University of São Paulo
- Emilio Hirsch
- Molecular Biotechnology Center, Department of Molecular Biotechnology and Health Sciences, University of Torino
- João S. Silva
- Department of Biochemistry and Immunology, Fiocruz- Bi-Institutional Translational Medicine Plataform, Ribeirão Preto Medical School, University of Sao Paulo
- Thiago M. Cunha
- Department of Pharmacology, Ribeirão Preto Medical School, University of Sao Paulo
- DOI
- https://doi.org/10.1038/s41467-018-03986-3
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 14
Abstract
Trypanosoma cruzi infection causes Chagas disease, but mechanisms underlying pathogenesis are unclear. Here, Silva et al. show that canonical PI3Kγ signaling in myeloid cells restricts T. cruzi infection in mice and that high PIK3CG expression correlates with low parasite levels in human Chagas’ hearts.
