Trypanosoma cruzi infection induces a global host cell response in cardiomyocytes
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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E-Artikel |
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2011 |
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2011 |
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Zur Gesamtaufnahme - volume:79 |
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Enthalten in: |
Infection and immunity - 79(2011), 5 vom: 22. Mai, Seite 1855-62 |
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Englisch |
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Beteiligte Personen: |
Manque, Patricio A [VerfasserIn] |
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Date Completed 23.06.2011 Date Revised 20.10.2021 published: Print-Electronic ErratumIn: Infect Immun. 2011 Aug;79(8):3471 Probst, Christian [corrected to Probst, Christian M]; Ozaki, L Shozo [corrected to Ozaki, Luiz Shozo] Citation Status MEDLINE |
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doi: |
10.1128/IAI.00643-10 |
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PPN (Katalog-ID): |
NLM206074220 |
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520 | |a 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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700 | 1 | |a Probst, Christian M |e verfasserin |4 aut | |
700 | 1 | |a Probst, Christian |e verfasserin |4 aut | |
700 | 1 | |a Pereira, Mirian C S |e verfasserin |4 aut | |
700 | 1 | |a Rampazzo, Rita C P |e verfasserin |4 aut | |
700 | 1 | |a Ozaki, Luiz Shozo |e verfasserin |4 aut | |
700 | 1 | |a Ozaki, L Shozo |e verfasserin |4 aut | |
700 | 1 | |a Pavoni, Daniela P |e verfasserin |4 aut | |
700 | 1 | |a Silva Neto, Dayse T |e verfasserin |4 aut | |
700 | 1 | |a Carvalho, M Ruth |e verfasserin |4 aut | |
700 | 1 | |a Xu, Ping |e verfasserin |4 aut | |
700 | 1 | |a Serrano, Myrna G |e verfasserin |4 aut | |
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700 | 1 | |a Meirelles, Maria de Nazareth S L |e verfasserin |4 aut | |
700 | 1 | |a Goldenberg, Samuel |e verfasserin |4 aut | |
700 | 1 | |a Krieger, Marco A |e verfasserin |4 aut | |
700 | 1 | |a Buck, Gregory A |e verfasserin |4 aut | |
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