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E-GEOD-6688

ABSTRACT: Transcription profiling of lungs from wild type and MyD88 knockout mice infected with Chlamydia pneumoniae to explore the influence of MyD88 on induction of immune responses.

OTHER RELATED OMICS DATASETS IN: PRJNA99067PRJNA99071

PROVIDER: E-GEOD-6688 | ExpressionAtlas | 2015-10-13

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-6688-analysis-methods.tsv	Tabular
	E-GEOD-6688-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-6688-configuration.xml	Xml
	E-GEOD-6688-percentile-ranks.tsv	Tabular
	E-GEOD-6688.condensed-sdrf.tsv	Tabular

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Similar Datasets

Transcription profiling of lungs from wild type and MyD88 knockout mice infected with Chlamydia pneumoniae to explore the influence of MyD88 on induction of immune responses.

Project description:Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule MyD88 play a critical role in inducing immunity against this microorganism and are crucial to survive the infection. To explore the influence of MyD88 on induction of immune responses in vivo on a genome wide level, WT or MyD88-/- mice were infected with C. pneumoniae upon anesthesia and the pulmonary transcriptome was analyzed three days later by microarrays. We find that the infection induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88-/- mice. This cluster contains primarily genes encoding for chemokines, cytokines and other immune effector molecules. Genes induced by interferons were abundant in a cluster of 102 genes which were only partially MyD88-dependent. Interestingly, a set of 37 genes were induced more strongly in MyD88-/- mice and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome upon infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses, and identified MyD88-independent genes involved in cellular replication Experiment Overall Design: Microarray analysis was performed in biological triplicates with RNA from individual mice derived from three independent infection experiments. Samples were lungs from wt and myd88 knock out mice, three days after Chlamydia pneumoniae or mock infection. Altogther 12 samples were analyzed on Affymetrix MOE430A arrays.

2007-11-15 | E-GEOD-6688 | biostudies-arrayexpress

MyD88-dependent changes in the pulmonary transcriptome after infection with Chlamydia pneumoniae

Project description:Chlamydia pneumoniae, an obligate intracellular bacterium, causes pneumonia in humans and mice. Toll-like receptors and the key adaptor molecule MyD88 play a critical role in inducing immunity against this microorganism and are crucial to survive the infection. To explore the influence of MyD88 on induction of immune responses in vivo on a genome wide level, WT or MyD88-/- mice were infected with C. pneumoniae upon anesthesia and the pulmonary transcriptome was analyzed three days later by microarrays. We find that the infection induced the transcription of 360 genes and repressed 18 genes in WT mice. Of these, 221 genes were not or weakly induced in lungs of MyD88-/- mice. This cluster contains primarily genes encoding for chemokines, cytokines and other immune effector molecules. Genes induced by interferons were abundant in a cluster of 102 genes which were only partially MyD88-dependent. Interestingly, a set of 37 genes were induced more strongly in MyD88-/- mice and most of them are involved in the regulation of cellular replication. In summary, ex vivo analysis of the pulmonary transcriptome upon infection with C. pneumoniae demonstrated a major impact of MyD88 on inflammatory responses but not on interferon-type responses, and identified MyD88-independent genes involved in cellular replication Keywords: lung, Chlamydia pneumoniae, mice, myd88, TLR, infection, knock out

2007-03-27 | GSE6688 | GEO

ANA-1 macrophages infected with Chlamydia pneumoniae

Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Keywords: Chlamydia pneumoniae, ANA-1 macrophages, in vitro, infection

2007-03-27 | GSE6690 | GEO

Gene signature profiles in lung tisses of wild type mice or PD-1 or PD-L1 deficient mice infected with Mycobacterium avium

Project description:Rationale: T cell activation is a key antimicrobial component against mycobacterial disease. Programmed cell death-1 (PD-1) and programmed cell death-ligand 1 (PD-L1) pathway could affect the antimicrobial immune responses by suppressing T cell activity. Several recent studies demonstrated that blocking of PD-1/PD-L1 pathway exacerbated Mycobacterium tuberculosis infection. However, the influence of blocking this pathway in pulmonary Mycobacterium avium-intracellulare complex (MAC) infection was not fully understood. Objective: We aimed to determine the influence of genetic depletion of PD-1/PD-L1 pathway on the disease activity of MAC infection. Methods: Wild-type, PD-1-deficient mice and PD-L1-deficient mice were intranasally infected with Mycobacterium avium bacteria. Measurements and Main Results: The depletion of PD-1 or PD-L1 did not affect mortality and bacterial burden in mice infected with MAC. However, remarkable infiltration of CD8 T lymphocytes was observed in the lungs of PD-1 and PD-L1 deficient mice compared to wild-type mice. Comprehensive transcriptome analysis showed that levels of gene expressions related to Th1 immunity did not differ according to the genotypes. However, genes related to the activity of CD8 T cells and related chemokine activity were up-regulated in the infected lungs of PD-1 and PD-L1 deficient mice. Conclusions: Depletion of PD-1/PD-L1 pathway did not affect the activation of Th1 immunity in response to MAC infection, which may explain why MAC infection was controlled in these mice. In addition, CD8-positive T cell pulmonary inflammation in knockout mice might have some clinical implication in the treatment of cancer patients with immune checkpoint inhibitors when the patients are infected with MAC.

2021-09-15 | GSE169202 | GEO

Transcription profiling of mouse ANA-1 macrophages infected with Chlamydia pneumoniae

Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Experiment Overall Design: ANA-1 macrophages were infected with Chlamydia pneumoniae or left untreated. After 8h total RNA was extracted. Two biological replicates were performed resulting in 4 arrays in total

2008-06-15 | E-GEOD-6690 | biostudies-arrayexpress

Urine metabolomic profiling of diabetic nephropathy in the steptozotocin induced type-1 diabetes mouse model.

Project description:This metabolomics study evaluated urine from wild-type and meprin β knockout mice after induction of diabetes with streptozotocin or treatment with sodium citrate control to understand how these factors influence the metabotype.

2017-02-17 | ST000559 | MetabolomicsWorkbench

Plasma metabolomic profiling of diabetic nephropathy in the steptozotocin induced type-1 diabetes mouse model

Project description:This metabolomics study evaluated plasma from wild-type and meprin β knockout mice after induction of diabetes with streptozotocin or treatment with sodium citrate control to understand how these factors influence the metabotype.

2017-02-17 | ST000558 | MetabolomicsWorkbench

Kidney tissue metabolomic profiling of diabetic nephropathy in the steptozotocin induced type-1 diabetes mouse model.

Project description:This metabolomics study evaluated kidney tissue from wild-type and meprin β knockout mice after induction of diabetes with streptozotocin or treatment with sodium citrate control to understand how these factors influence the metabotype.

2017-01-20 | ST000540 | MetabolomicsWorkbench

The effect of bacterial capsule on macrophage transcriptional responses to Streptococcus Pneumoniae.

Project description:Streptococcus Pneumoniae capsule is a major virulence factor. The capsule is known to inhibit complement fixation and phagocytes, but its impact on innate immune responses is not known. To address this question, we compared transcriptional responses by human monocyte derived macrophages in responses to wild type S. pneumoniae with isogenic mutant bacteria lacking their capsule. We conducted these experiments with and without macrophage pretreatment with cytochalasin D to evaluate the impact of phagocytosis, and we also made comparisons to mutant S.pneumoniae lacking bacterial lipoprotein which is known to be necessary for maximal innate immune responses.

2018-04-02 | E-MTAB-5894 | biostudies-arrayexpress

Trancriptome profiling of murine lung after pneumococcal respiratory infection, antibiotic administation, and treatment with immunostimulants

Project description:The study aimed at defining the transcriptional responses of the respiratory tract after respiratory infection with Streptococcus pneumoniae, treatment with antibiotic and administration of immunostimulatory molecules. For this purpose, mice were infected by intranasal route with S. pneumoniae. After 12h, animals were treated by orogastric administration of amoxicillin and either intraperitoneal injection of monophosphoryl lipid A or intranasal instillation of flagellin FliC∆174-400. Whole lungs were then sampled at selected times for microarray analyses.

2021-07-29 | GSE118860 | GEO

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