Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling
<p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves...
Ausführliche Beschreibung
Autor*in: |
Burleigh Barbara A [verfasserIn] Daily Johanna P [verfasserIn] Costales Jaime A [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2009 |
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Übergeordnetes Werk: |
In: BMC Genomics - BMC, 2003, 10(2009), 1, p 252 |
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Übergeordnetes Werk: |
volume:10 ; year:2009 ; number:1, p 252 |
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DOI / URN: |
10.1186/1471-2164-10-252 |
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Katalog-ID: |
DOAJ048531790 |
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520 | |a <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< | ||
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10.1186/1471-2164-10-252 doi (DE-627)DOAJ048531790 (DE-599)DOAJ0fca395df7ec4731b7289bc55ed33fc6 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Burleigh Barbara A verfasserin aut Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< Biotechnology Genetics Daily Johanna P verfasserin aut Costales Jaime A verfasserin aut In BMC Genomics BMC, 2003 10(2009), 1, p 252 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:10 year:2009 number:1, p 252 https://doi.org/10.1186/1471-2164-10-252 kostenfrei https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 kostenfrei http://www.biomedcentral.com/1471-2164/10/252 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1, p 252 |
spelling |
10.1186/1471-2164-10-252 doi (DE-627)DOAJ048531790 (DE-599)DOAJ0fca395df7ec4731b7289bc55ed33fc6 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Burleigh Barbara A verfasserin aut Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< Biotechnology Genetics Daily Johanna P verfasserin aut Costales Jaime A verfasserin aut In BMC Genomics BMC, 2003 10(2009), 1, p 252 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:10 year:2009 number:1, p 252 https://doi.org/10.1186/1471-2164-10-252 kostenfrei https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 kostenfrei http://www.biomedcentral.com/1471-2164/10/252 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1, p 252 |
allfields_unstemmed |
10.1186/1471-2164-10-252 doi (DE-627)DOAJ048531790 (DE-599)DOAJ0fca395df7ec4731b7289bc55ed33fc6 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Burleigh Barbara A verfasserin aut Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< Biotechnology Genetics Daily Johanna P verfasserin aut Costales Jaime A verfasserin aut In BMC Genomics BMC, 2003 10(2009), 1, p 252 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:10 year:2009 number:1, p 252 https://doi.org/10.1186/1471-2164-10-252 kostenfrei https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 kostenfrei http://www.biomedcentral.com/1471-2164/10/252 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1, p 252 |
allfieldsGer |
10.1186/1471-2164-10-252 doi (DE-627)DOAJ048531790 (DE-599)DOAJ0fca395df7ec4731b7289bc55ed33fc6 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Burleigh Barbara A verfasserin aut Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< Biotechnology Genetics Daily Johanna P verfasserin aut Costales Jaime A verfasserin aut In BMC Genomics BMC, 2003 10(2009), 1, p 252 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:10 year:2009 number:1, p 252 https://doi.org/10.1186/1471-2164-10-252 kostenfrei https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 kostenfrei http://www.biomedcentral.com/1471-2164/10/252 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1, p 252 |
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10.1186/1471-2164-10-252 doi (DE-627)DOAJ048531790 (DE-599)DOAJ0fca395df7ec4731b7289bc55ed33fc6 DE-627 ger DE-627 rakwb eng TP248.13-248.65 QH426-470 Burleigh Barbara A verfasserin aut Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< Biotechnology Genetics Daily Johanna P verfasserin aut Costales Jaime A verfasserin aut In BMC Genomics BMC, 2003 10(2009), 1, p 252 (DE-627)326644954 (DE-600)2041499-7 14712164 nnns volume:10 year:2009 number:1, p 252 https://doi.org/10.1186/1471-2164-10-252 kostenfrei https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 kostenfrei http://www.biomedcentral.com/1471-2164/10/252 kostenfrei https://doaj.org/toc/1471-2164 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1, p 252 |
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Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling |
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Burleigh Barbara A |
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BMC Genomics |
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eng |
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2009 |
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Burleigh Barbara A Daily Johanna P Costales Jaime A |
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10 |
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TP248.13-248.65 QH426-470 |
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Elektronische Aufsätze |
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Burleigh Barbara A |
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10.1186/1471-2164-10-252 |
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verfasserin |
title_sort |
cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<trypanosoma cruzi</it<-infected host cells by comparative mrna profiling |
callnumber |
TP248.13-248.65 |
title_auth |
Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling |
abstract |
<p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< |
abstractGer |
<p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< |
abstract_unstemmed |
<p<Abstract</p< <p<Background</p< <p<The requirements for growth and survival of the intracellular pathogen <it<Trypanosoma cruzi </it<within mammalian host cells are poorly understood. Transcriptional profiling of the host cell response to infection serves as a rapid read-out for perturbation of host physiology that, in part, reflects adaptation to the infective process. Using Affymetrix oligonucleotide array analysis we identified common and disparate host cell responses triggered by <it<T. cruzi </it<infection of phenotypically diverse human cell types.</p< <p<Results</p< <p<We report significant changes in transcript abundance in <it<T. cruzi</it<-infected fibroblasts, endothelial cells and smooth muscle cells (2852, 2155 and 531 genes respectively; fold-change ≥ 2, p-value < 0.01) 24 hours post-invasion. A prominent type I interferon response was observed in each cell type, reflecting a secondary response to secreted cytokine in infected cultures. To identify a core cytokine-independent response in <it<T. cruzi</it<-infected fibroblasts and endothelial cells transwell plates were used to distinguish cytokine-dependent and -independent gene expression profiles. This approach revealed the induction of metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding as common themes in <it<T. cruzi</it<-infected cells. In addition, the downregulation of genes involved in mitotic cell cycle and cell division predicted that <it<T. cruzi </it<infection may impede host cell cycle progression. The observation of impaired cytokinesis in <it<T. cruzi</it<-infected cells, following nuclear replication, confirmed this prediction.</p< <p<Conclusion</p< <p<Metabolic pathways and cellular processes were identified as significantly altered at the transcriptional level in response to <it<T. cruzi </it<infection in a cytokine-independent manner. Several of these alterations are supported by previous studies of <it<T. cruzi </it<metabolic requirements or effects on the host. However, our methods also revealed a <it<T. cruzi</it<-dependent block in the host cell cycle, at the level of cytokinesis, previously unrecognized for this pathogen-host cell interaction.</p< |
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title_short |
Cytokine-dependent and–independent gene expression changes and cell cycle block revealed in <it<Trypanosoma cruzi</it<-infected host cells by comparative mRNA profiling |
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https://doi.org/10.1186/1471-2164-10-252 https://doaj.org/article/0fca395df7ec4731b7289bc55ed33fc6 http://www.biomedcentral.com/1471-2164/10/252 https://doaj.org/toc/1471-2164 |
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