Patterns of gene expression associated with temporal phases of S. aureus infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE25244 | GEO | 2011/08/03
SECONDARY ACCESSION(S): PRJNA134659
REPOSITORIES: GEO
Similar Datasets
Project description:To acquire more information regarding the local immune events during the different phases of S. aureus infection, gene profiling using microarray technology was used to identify host genes whose expression is substantively altered in the kidneys during the acute (T2) and persistent phase of infection (T28). Genes associated with the distinct transcript profiles were identified by comparing the relative abundance of transcripts at 2 days (acute) and 28 days (persistent) of infection to their abundance in the kidneys of uninfected control animals (CTL). Keywords: gene expression identification of host genes whose expression is substantively altered in the kidneys during the acute (T2) and persistent phase of infection (T28) compared to uninfected control (CTL).
2011-08-02 | E-GEOD-25244 | biostudies-arrayexpress
Project description:Cytolytic activity by CD8+ cytotoxic T lymphocytes (CTL) is a powerful tactic in the elimination of intracellular pathogens and tumor cells. The destructive capacity of CTL is progressively dampened during chronic infection - yet the environmental cues and molecular pathways controlling immune “exhaustion” remain unclear. We find CTL immunity is regulated by the central transcriptional response to hypoxia, mediated by the von-Hippel-Lindau/Hypoxia-Inducible-Factor (VHL/HIF) pathway. Deletion of VHL, the primary negative regulator of HIF, leads to lethal CTL-mediated immunopathology during chronic infection, and VHL-deficient CTL display enhanced control of persistent viral infection and neoplastic growth. We find HIF and oxygen influence expression of pivotal CTL transcription, effector and costimulatory-inhibitory molecules, which is relevant to strategies to promote viral and tumor clearance. To understand the role of the VHL/HIF pathway in regulating T cell responses to acute and persistant antigen in vivo, a mixture of ~10^4 WT and Vhl KO virus-specific CD8+ T cells (P14s) was transferred iv into uninfected WT host mice. After infection with either LCMV-Armstrong (acute viral infection) or LCMV-clone13 (persistent viral infection) we double-FACS isolated the responding P14 donor cells from pooled spleens from two sets of host mice to obtain duplicates for microarray for the four conditions, resulting in eight samples (2 WT Arm, 2 VHL KO Arm; 2 WT cl13, 2 VHL KO cl13) at 6 to 7 days post-infection. All conditions were sorted on KRLG1lo P14 cells. Note this was a mixed P14 transfer, so WT and KO cells were responding to infection in the same WT host mice to aid in normalizing effects such as antigen load and cytokine environment.
2013-09-29 | E-GEOD-50158 | biostudies-arrayexpress
Project description:Cytolytic activity by CD8+ cytotoxic T lymphocytes (CTL) is a powerful tactic in the elimination of intracellular pathogens and tumor cells. The destructive capacity of CTL is progressively dampened during chronic infection - yet the environmental cues and molecular pathways controlling immune “exhaustion” remain unclear. We find CTL immunity is regulated by the central transcriptional response to hypoxia, mediated by the von-Hippel-Lindau/Hypoxia-Inducible-Factor (VHL/HIF) pathway. Deletion of VHL, the primary negative regulator of HIF, leads to lethal CTL-mediated immunopathology during chronic infection, and VHL-deficient CTL display enhanced control of persistent viral infection and neoplastic growth. We find HIF and oxygen influence expression of pivotal CTL transcription, effector and costimulatory-inhibitory molecules, which is relevant to strategies to promote viral and tumor clearance.
2013-09-29 | GSE50158 | GEO
Project description:Purpose: Gut microbiota is associated with the progression of brain tumor. However, the alterations in the gut microbiota during glioma growth and temozolomide (TMZ) therapy remains to be understood. Methods: C57BL/6 male mice were implanted with GL261 glioma cells. TMZ/sodium carboxymethyl cellulose (SCC) was administered by gavage for five consecutive days (from 8 to 12 days after implantation). Fecal samples were collected before (T0) and on days 7 (T1), 14 (T2), and 28 (T3) after implantation. The gut microbiota was analyzed using 16S ribosomal DNA sequencing followed by absolute and relative quantitation analyses. Results: Nineteen genera were altered during glioma progression with the most dramatic changes in Firmicutes and Bacteroidetes phyla. During glioma growth, Lactobacillus abundance decreased at the earlier stage of glioma development (T1), and then gradually increased (T2, T3); Intestinimonas abundance exhibited a persistent increase; Anaerotruncus showed a transient increase and then a subsequent decrease. Twenty genera altered following TMZ treatment. The enrichment of Akkermansia and Bifidobacterium was observed only at the early stage following TMZ treatment (T2), but not at the later stage (T3). Additionally, the decrease of Anaerotruncus was slighter in TMZ group at T3 comparing to the vehicle group. The abundance of Intestinimonas increased constantly during the progression of glioma, but was unaffected by TMZ. Conclusions: Glioma development and progression resulted in altered gut microbiota. TMZ reversed the decrease of Anaerotruncus in glioma at T3, and increased the abundance of Bifidobacterium with no influence on the increase of Intestinimonas. Short-term and long-term effects of TMZ treatment on the bacterial communities may be differential. This study will improve understanding the role of gut microbiota in glioma, and help develop gut microbiota as a potential therapeutic target.
2021-04-28 | GSE171041 | GEO
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2010-06-25 | BIOMD0000000686 | BioModels
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2010-06-25 | BIOMD0000000688 | BioModels
Project description:This a model from the article:
Dynamics of killer T cell inflation in viral infections.
Wodarz D, Sierro S, Klenerman P. J R Soc Interface
2007 Jun 22;4(14):533-43 17251133
,
Abstract:
Upon acute viral infection, a typical cytotoxic T lymphocyte (CTL) response is
characterized by a phase of expansion and contraction after which it settles at
a relatively stable memory level. Recently, experimental data from mice infected
with murine cytomegalovirus (MCMV) showed different and unusual dynamics. After
acute infection had resolved, some antigen specific CTL started to expand over
time despite the fact that no replicative virus was detectable. This phenomenon
has been termed as "CTL memory inflation". In order to examine the dynamics of
this system further, we developed a mathematical model analysing the impact of
innate and adaptive immune responses. According to this model, a potentially
important contributor to CTL inflation is competition between the specific CTL
response and an innate natural killer (NK) cell response. Inflation occurs most
readily if the NK cell response is more efficient than the CTL at reducing virus
load during acute infection, but thereafter maintains a chronic virus load which
is sufficient to induce CTL proliferation. The model further suggests that
weaker NK cell mediated protection can correlate with more pronounced CTL
inflation dynamics over time. We present experimental data from mice infected
with MCMV which are consistent with the theoretical predictions. This model
provides valuable information and may help to explain the inflation of CMV
specific CD8+T cells seen in humans as they age.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Wodarz D, Sierro S, Klenerman P. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2010-06-25 | BIOMD0000000687 | BioModels
Project description:Comparison of the transcriptiomic profiles using DNA microarray analysis betwween the pharyneal (target of FMDV acute and persistent infection) and lung (target of FMDV acute infection) tissues of cattle
2023-09-01 | GSE232440 | GEO
Project description:Background: Dengue virus (DENV) infection often leads to acute illness lasting 2-7 days with severity ranging from dengue fever (DF) to hemorrhagic fever (DHF) and fatal dengue shock syndrome (DSS). The dynamic changes of host responses on the gene transcription level that accompany DENV infection and differences between DF and DHF cases have been poorly understood, particularly for South American population. Methodology/Principal Findings: Supported by a longitudinal active surveillance program for dengue transmission in Maracay, Venezuela, we conducted a prospective study to investigate host responses in dengue patients. Blood specimens and clinical information were collected on a daily basis from febrile cases confirmed with DENV infection from their first day of enrollment to early defervescence together with one convalescent sample. A total of 49 and 13 study participants were defined as DF and DHF cases respectively based on their clinical and hematological information. Using convalescent specimens as baseline, day-to-day gene expression was evaluated ex vivo in peripheral blood mononuclear cells of the study participants. Two waves of gene expression were detected: the first wave peaked at day 1 from the onset of fever (day 0) then declined at days 3-4; the second wave emerged from day 4 and peaked around day 5-6. Genes associated with innate immune process, including type I interferon signaling, cytokine-mediated signaling, chemotaxis, and antiviral responses, dominated the first wave; whereas genes involved in cell cycle processes, including cell division, mitosis, DNA replication, chromosome, and spindle organization dominated the second wave. Measureable genomic markers predicted early acute, late acute and convalescent phases with 91% accuracy. Gene signatures expressed in early acute phase predicted disease severity (DF vs DHF) with 96% accuracy. Conclusions/Significance: Our study established a dynamic pattern of detailed host immune responses to DENV infection and revealed genomic signatures valuable for diagnostics purposes.
2013-01-26 | GSE43777 | GEO
Project description:Gene expression profiles were examined in whole lung tissue collected from male and female Long-Evans rats at different time points after inoculation with Seoul virus (i.e., the species-specific hantavirus that infects Norway rats); We used microarray analyses to analyze global gene expression differences between the sexes during hantavirus infection Experiment Overall Design: Gonadally-intact male and female rats were inoculated with 10^4 pfu of Seoul virus (strain SR-11) and lung samples were collected 0, 3, 15, and 40 days post-inoculation (p.i.) to assess gene expression patterns during the acute (i.e., days 3-15 p.i.) and persistent (i.e., day 40 p.i.) phases of infection
2008-06-15 | E-GEOD-7271 | biostudies-arrayexpress