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Expression data of LPS-stimulated macrophages in wild-type and LysM-Cre+;Akirin2fl/fl mice

ABSTRACT: Akirin2 is an evolutionally conserved nuclear protein involved in the regulation of a set of inflammatory gene expression in various cell types. We used microarrays to examine the effect of Akirin2 deficiency in LPS-inducible gene expression in macrophages

ORGANISM(S): Mus musculus

PROVIDER: GSE59319 | GEO | 2014/07/11

SECONDARY ACCESSION(S): PRJNA255051

REPOSITORIES: GEO

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Expression data of LPS-stimulated macrophages in wild-type and LysM-Cre+;Akirin2fl/fl mice

Project description:Akirin2 is an evolutionally conserved nuclear protein involved in the regulation of a set of inflammatory gene expression in various cell types. We used microarrays to examine the effect of Akirin2 deficiency in LPS-inducible gene expression in macrophages Peritoneal macrophages from wild-type and LysM-Cre+;Akirin2fl/fl mice were stimulated with LPS for 0, 2 and 4 hours, followed by RNA extraction and microarray analysis.

2014-07-11 | E-GEOD-59319 | biostudies-arrayexpress

Expression data of LPS-stimulated macrophages from wild-type and Zc3h12a-/- mice.

2009-02-19 | GSE14891 | GEO

Expression data of LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- mice.

2009-02-19 | GSE14890 | GEO

Transcription profiling of mouse LPS-stimulated macrophages from wild-type and Zc3h12a-/- knockouts

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, induces the expression of various genes including proinflammatory cytokines, and the expression is modified by the presence of Zc3h12a. We used microarrays to examine influence of Zc3h12a deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type and Zc3h12a-/- mice were stimulated with LPS for 0, 1, 2 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14891 | biostudies-arrayexpress

Transcription profiling of mouse LPS-stimulated macrophages from wild-type, MyD88-/- and TRIF-/- animals

Project description:Lipopolysaccharide (LPS), a Toll-like receptor (TLR) 4 ligand, activates intracellular signaling via adaptors, MyD88 and TRIF, leading to the expression of various genes including proinflammatory cytokines. We used microarrays to examine influence of MyD88 or TRIF deficiency in LPS-inducible gene expression. Experiment Overall Design: Peritoneal macrophages from wild-type, MyD88-/- and TRIF-/- mice were stimulated with LPS for 0, 1 and 4 hours, followed by RNA extraction. Then hybridization on affymetrix microarrays was performed.

2009-03-01 | E-GEOD-14890 | biostudies-arrayexpress

Expression data from LysMCre/Cre and KLF2∆/∆ (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with LPS for 6hours

Project description:Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.

2012-04-16 | GSE26727 | GEO

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

Transcription profiling by array of LysMCre/Cre and KLF2?/? (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with lipopolysaccharide (LPS) for 6 hours

Project description:Gene expression profile of LysMCre/Cre and KLF2?/? primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2?/? primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation. We injected 3 pairs of LysMCre/Cre (n=3) and KLF2?/? (n=3) mice with 2 ml of thioglycolate broth intraperitoneally. After 72 hours of thioglycolate injection, total cell suspension from peritoneal cavity were collected. These cells were seeded on 100mm tissue culture plates. Cells were allowed to attach for 4 hours and unattached cells were removed by washing with cell culture medium. These cells were placed in humidified incubator for additional 24 hours before LPS treatment. LPS was diluted to final concentration of 100ng/ml in culture medium and this medium was placed on peritoneal macrophages derived from LysM Cre/Cre and KLF2?/? mice for 6hours. Cells were lysed and total RNA was isolated and subjected to hybridization on Affymetrix microarrays.

2012-04-15 | E-GEOD-26727 | biostudies-arrayexpress

Gene Expression in Naive and Tolerant Macrophages stimulated with LPS

Project description:The inflammatory response initiated by microbial products signaling through Toll-like receptors (TLRs) of the innate immune system is essential for host defense against infection. Because inflammation can be harmful to host tissues, the innate response is highly regulated. Negative regulation of TLR4, the receptor for bacterial lipopolysaccharide (LPS), results in LPS tolerance, defined as hyporesponsiveness to repeated stimulation with LPS. LPS tolerance is thought to protect the host from excessive inflammation by turning off TLR4 signal, which then shuts down TLR-induced genes. However, TLR signaling induces hundreds of genes with very different functions. We reasoned that genes with different functions should have different requirements for regulation. Specifically, genes encoding proinflammatory mediators should be transiently inactivated to limit tissue damage, while genes encoding antimicrobial effectors, which directly target pathogens, should remain inducible in tolerant cells to protect the host from infection. Using an in vitro system of LPS tolerance in macrophages, here we show that TLR-induced genes may indeed be divided into two distinct categories based on their functions and regulatory requirements. Further, we show these distinct groups are regulated by gene-specific, and not signal-specific mechanisms. Keywords: Treatment Comparison

2007-04-22 | GSE7348 | GEO

Differential gene expression analysis for BAL cells isolated from LysM Cre and Netrin1loxp/loxp LysM Cre mice after intratracheal LPS challenge

Project description:Purpose: The goal of this study is to compare NGS-derived transcriptome profiling (mRNA-seq) of expressed genes between LysM Cre and Netrin1loxp/loxp LysM Cre mice 3 days after intratracheal LPS challenge in order to explain the worsened outcomes and increased levels of inflammation we measure in the Netrin1loxp/loxp LysM Cre mice Methods: Three days after mice were treated with intratracheal injections of LPS, BAL cells were collected and then depleted for neutrophils using antibody-mediated depletion. The remaining cells were used for RNA isolation. mRNA profiles were generated by deep sequencing, in quadruplicate (one sample in the Netrin1loxp/loxp LysM Cre group was excluded as the sequence depth was only half compare to other 3 replicates), using paired-end 75-cycle sequencing on an Illumina NextSeq 550 System. Bases with quality scores < 20 and adapter sequences were removed from raw data with Cutadapt (v1.15), followed by alignment of clean RNA-seq reads to GRCm38 with STAR(v2.5.3a). Gene abundance was counted by HTseq-count uniquely-mapped reads number with default parameter using GencodeM15. Genes with > 5 reads in at least one sample were included for differential expression analysis by DESeq2 software.

2021-02-24 | GSE167333 | GEO

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