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 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< Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Burleigh Barbara A [verfasserIn] Daily Johanna P [verfasserIn] Costales Jaime A [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Übergeordnetes Werk:	In: BMC Genomics - BMC, 2003, 10(2009), 1, p 252
Übergeordnetes Werk:	volume:10 ; year:2009 ; number:1, p 252

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1471-2164-10-252

Katalog-ID:	DOAJ048531790

Internformat


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allfields	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
allfieldsSound	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
language	English
source	In BMC Genomics 10(2009), 1, p 252 volume:10 year:2009 number:1, p 252
sourceStr	In BMC Genomics 10(2009), 1, p 252 volume:10 year:2009 number:1, p 252
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Biotechnology Genetics
isfreeaccess_bool	true
container_title	BMC Genomics
authorswithroles_txt_mv	Burleigh Barbara A @@aut@@ Daily Johanna P @@aut@@ Costales Jaime A @@aut@@
publishDateDaySort_date	2009-01-01T00:00:00Z
hierarchy_top_id	326644954
id	DOAJ048531790
language_de	englisch
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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. 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author	Burleigh Barbara A
spellingShingle	Burleigh Barbara A misc TP248.13-248.65 misc QH426-470 misc Biotechnology misc Genetics 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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topic_title	TP248.13-248.65 QH426-470 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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title	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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title_full	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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author_browse	Burleigh Barbara A Daily Johanna P Costales Jaime A
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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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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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