Immediate/Early Response to Trypanosoma cruzi Infection Involves Minimal Modulation of Host Cell Transcription
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE3476 | GEO | 2005/10/20
SECONDARY ACCESSION(S): PRJNA93285
REPOSITORIES: GEO
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Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of approximately 27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced > or =2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFNbeta at 18 hpi following the induction of IFNbeta transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
2005-09-26 | E-SMDB-1563 | biostudies-arrayexpress
Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of approximately 27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced > or =2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFNbeta at 18 hpi following the induction of IFNbeta transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
2005-09-26 | E-SMDB-1561 | biostudies-arrayexpress
Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of approximately 27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced > or =2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFNbeta at 18 hpi following the induction of IFNbeta transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
2005-09-26 | E-SMDB-1562 | biostudies-arrayexpress
Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of approximately 27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced > or =2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFNbeta at 18 hpi following the induction of IFNbeta transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-10-20 | E-GEOD-3476 | biostudies-arrayexpress
Project description:Host cell infection by the intracellular pathogen, Trypanosoma cruzi, involves activation of signaling pathways, cytoskeletal reorganization, and targeted recruitment of host cell lysosomes. To determine the consequences of T. cruzi invasion on host cell gene expression, high density microarrays consisting of ~27,000 human cDNAs were hybridized with fluorescent probes generated from T. cruzi-infected human fibroblasts (HFF) at early time points following infection (2-24 h). Surprisingly, no genes were induced 2-fold in HFF between 2 and 6 h post-infection (hpi) in repeated experiments while immediate repression of six host cell transcripts was observed. A significant increase in transcript abundance for 106 host cell genes was observed at 24 hpi. Among the most highly induced is a set of interferon-stimulated genes, indicative of a type I interferon (IFN) response to T. cruzi. In support of this, T. cruzi-infected fibroblasts begin to secrete IFN at 18 hpi following the induction of IFN transcripts. As compared with global transcriptional responses evoked by other intracellular pathogens, T. cruzi is a stealth parasite that elicits few changes in host cell transcription during the initiation of infection.
2005-09-26 | E-SMDB-1560 | biostudies-arrayexpress
Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Keywords: infection response
2008-02-06 | GSE7047 | GEO
Project description:As Trypanosoma cruzi, the etiological agent of Chagas disease, multiplies in the cytoplasm of nucleated host cells, infection with this parasite is highly likely to affect host cells. We performed an exhaustive transcriptome analysis of T. cruzi-infected HeLa cells using an oligonucleotide microarray containing probes for greater than 47,000 human gene transcripts. In comparison with uninfected cells, those infected with T. cruzi showed greater than threefold up-regulation of 41 genes and greater than threefold down-regulation of 23 genes. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of selected, differentially expressed genes confirmed the microarray data. Many of these up- and down-regulated genes were related to cellular proliferation, including seven up-regulated genes encoding proliferation inhibitors and three down-regulated genes encoding proliferation promoters, strongly suggesting that T. cruzi infection inhibits host cell proliferation, which may allow more time for T. cruzi to replicate and produce its intracellular nests. These findings provide new insight into the molecular mechanisms by which intracellular T. cruzi infection influences the host cell, leading to pathogenicity. Experiment Overall Design: Three replicates of infected and uninfected HeLa cell were analyzed. To examine the extent of cross hybridization between T. cruzi cRNA and Human chip, trypomastigote cRNA was hybridized with the same chip.
2008-04-08 | E-GEOD-7047 | biostudies-arrayexpress
Project description:Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunocompromised and immunosuppressed individuals. During infection, HCMV is known to employ host transcription factors to facilitate viral gene expression. To further understand the previously observed delayed viral replication and protein expression in p53 knockout cells, we conducted microarray analyses on p53+/+ and p53-/- immortalized fibroblast cell lines. At 12 hpi, applying the significance criteria defined above, no genes showed a significant difference in any of the comparisons. At 24 hpi, we found 19 genes to be significantly different in the THF versus p53-/- comparison and 14 genes to be significantly different in the HFF versus p53-/- comparison. Eleven genes were shared between HFF and THF cells when compared to p53-/- cells (UL30, UL54, UL63, UL65, UL69, UL75, UL110, UL122, IRL4, IRS1, TRS1, shown in bold in Table 1). Eight genes were unique in the THF versus p53-/- comparison (UL48, UL68, UL84, UL100, UL106, UL109, UL111, RL5A), and three genes in the HFF versus p53-/- cell comparison (UL14, UL16, US2). When comparing HFF and THF cells, only US2 showed a significant difference. The ratio (HFF versus p53-/- divided by THF versus p53-/-) of the expression levels of the eleven shared genes from the HFF versus p53-/- and THF versus p53-/- comparisons was an averaged 1.2, indicating that, with the exception of US2, these two cell lines behaved similarly with respect to p53-driven viral gene expression. Keywords: time course, virus, cytomegalo, hhv5, infection, p53
2008-12-01 | GSE13437 | GEO
Project description:Human cytomegalovirus (HCMV) is a common cause of morbidity and mortality in immunocompromised and immunosuppressed individuals. During infection, HCMV is known to employ host transcription factors to facilitate viral gene expression. To further understand the previously observed delayed viral replication and protein expression in p53 knockout cells, we conducted microarray analyses on p53+/+ and p53-/- immortalized fibroblast cell lines. At 12 hpi, applying the significance criteria defined above, no genes showed a significant difference in any of the comparisons. At 24 hpi, we found 19 genes to be significantly different in the THF versus p53-/- comparison and 14 genes to be significantly different in the HFF versus p53-/- comparison. Eleven genes were shared between HFF and THF cells when compared to p53-/- cells (UL30, UL54, UL63, UL65, UL69, UL75, UL110, UL122, IRL4, IRS1, TRS1, shown in bold in Table 1). Eight genes were unique in the THF versus p53-/- comparison (UL48, UL68, UL84, UL100, UL106, UL109, UL111, RL5A), and three genes in the HFF versus p53-/- cell comparison (UL14, UL16, US2). When comparing HFF and THF cells, only US2 showed a significant difference. The ratio (HFF versus p53-/- divided by THF versus p53-/-) of the expression levels of the eleven shared genes from the HFF versus p53-/- and THF versus p53-/- comparisons was an averaged 1.2, indicating that, with the exception of US2, these two cell lines behaved similarly with respect to p53-driven viral gene expression. Keywords: time course, virus, cytomegalo, hhv5, infection, p53 Each slide consisted of 4 arrays. Each array consisted of 305 control features, 1265 cellular gene features and 670 viral gene features. The study was performed on 6 slides (HFF-THF, HFF-p53-/-, THF-p53-/- at 12 and 24 hpi). 3 arrays per slide were hybridized with 3 biological replicates of labelled RNA, the 4th array was hybridized with an equimolar mixture of the 3 biological replicate samples. This array was used for control purposes only, and the results were not used for downstream calculations. Each slide was stripped and reprobed two times to provide 3 technical replicates of each sample. As our experiments concentrated on viral genes and their expression, cellular genes were not further analyzed in this study.
2010-05-15 | E-GEOD-13437 | biostudies-arrayexpress
Project description:Trypanosoma cruzi is an obligate intracellular protozoan parasite that causes human Chagas’ disease, a leading cause of heart failure in Latin America. Using Affymetrix oligonucleotide arrays we screened phenotypically diverse human cells (foreskin fibroblasts, microvascular endothelial cells and vascular smooth muscle cells) for a common transcriptional response signature to T. cruzi. A common feature was a prominent type I interferon response, indicative of a secondary response to secreted cytokines. Using transwell plates to distinguish cytokine-dependent and -independent gene expression profiles in T. cruzi-infected cells, a core cytokine-independent response was identified in fibroblasts and endothelial cells that featured metabolic and signaling pathways involved in cell proliferation, amino acid catabolism and response to wounding. Significant downregulation of genes involved in mitotic cell cycle and cell division predicted that T. cruzi infection impedes cell cycle progression in the host cell.
2009-06-04 | GSE13791 | GEO