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TRYPANOSOMA CRUZI INFECTION INDUCES A GLOBAL HOST CELL RESPONSE IN CARDIOMYOCYTES
Author
Manque, Patricio A.
Probst, Christian M.
Probst, Christian
Pereira, Mirian C. S.
Rampazzo, Rita C. P.
Ozaki, Luiz Shozo
Ozaki, L. Shozo
Pavoni, Daniela P.
Silva Neto, Dayse T.
Carvalho, M. Ruth
Xu, Ping
Serrano, Myrna G.
Alves, João M. P.
Meirelles, Maria de Nazareth S. L.
Goldenberg, Samuel
Krieger, Marco A.
Buck, Gregory A.
Probst, Christian M.
Probst, Christian
Pereira, Mirian C. S.
Rampazzo, Rita C. P.
Ozaki, Luiz Shozo
Ozaki, L. Shozo
Pavoni, Daniela P.
Silva Neto, Dayse T.
Carvalho, M. Ruth
Xu, Ping
Serrano, Myrna G.
Alves, João M. P.
Meirelles, Maria de Nazareth S. L.
Goldenberg, Samuel
Krieger, Marco A.
Buck, Gregory A.
Affilliation
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil / Instituto Carlos Chagas. Curitiba, PR, Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil / Instituto Carlos Chagas. Curitiba, PR, Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Rio de Janeiro, RJ. Brasil.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Instituto Carlos Chagas. Curitiba, PR, Brasil.
Virginia Commonwealth University. Center for the Study of Biological Complexity. Department of Microbiology and Immunology. Richmond, Virginia, USA.
Abstract
Chagas' disease, caused by the hemoflagellate protozoan Trypanosoma cruzi, affects millions of people in South and Central America. Chronic chagasic cardiomyopathy, the most devastating manifestation of this disease, occurs in approximately one-third of infected individuals. Events associated with the parasite's tropism for and invasion of cardiomyocytes have been the focus of intense investigation in recent years. In the present study, we use murine microarrays to investigate the cellular response caused by invasion of primary murine cardiomyocytes by T. cruzi trypomastigotes. These studies identified 353 murine genes that were differentially expressed during the early stages of invasion and infection of these cells. Genes associated with the immune response, inflammation, cytoskeleton organization, cell-cell and cell-matrix interactions, apoptosis, cell cycle, and oxidative stress are among those affected during the infection. Our data indicate that T. cruzi induces broad modulations of the host cell machinery in ways that provide insight into how the parasite survives, replicates, and persists in the infected host and ultimately defines the clinical outcome of the infection.
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