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Macrophage Response to Sendai virus infection.

ABSTRACT: Thus, mouse macrophage cultures were established from PBMCs isolated from wild-type control mice and were inoculated with SeV (Sendai virus) or UV-SeV (UV-inactivated SeV). These microarrays were performed in concert with assays of CCL5 and CCR5 expression, viral replication, and cellular apoptosis. Initial experiments indicated that wild-type mouse macrophages inoculated with SeV exhibit induction of CCL5 mRNA to the highest level of any known mouse gene product, while mRNA levels for CCL5 receptors (CCR5 as well as CCR3 and CCR1) or alternative ligands for these receptors (CCL3 and CCL4) were relatively unchanged by viral infection. Keywords: Treatment Comparison

ORGANISM(S): Mus musculus

PROVIDER: GSE2935 | GEO | 2005/10/10

SECONDARY ACCESSION(S): PRJNA92443

REPOSITORIES: GEO

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Transcription profiling of mouse macrophage response to sendai virus infection.

Project description:Thus, mouse macrophage cultures were established from PBMCs isolated from wild-type control mice and were inoculated with SeV (Sendai virus) or UV-SeV (UV-inactivated SeV). These microarrays were performed in concert with assays of CCL5 and CCR5 expression, viral replication, and cellular apoptosis. Initial experiments indicated that wild-type mouse macrophages inoculated with SeV exhibit induction of CCL5 mRNA to the highest level of any known mouse gene product, while mRNA levels for CCL5 receptors (CCR5 as well as CCR3 and CCR1) or alternative ligands for these receptors (CCL3 and CCL4) were relatively unchanged by viral infection. Experiment Overall Design: Macrophages were pooled from mice and subsequently cultured (~3 mice/well). Each culture well was then subjected to one of two treatments (SeV, or UV-SeV) for 4 days. Thus, per condition, N = 2 culture wells, with each well independently analyzed by microarray. No technical replicates were performed, but arrays were evaluated for quality control using the SimpleAffy package (Miller CJ, 2004) in Bioconductor 1.5.

2008-06-12 | E-GEOD-2935 | biostudies-arrayexpress

Airway Epithelial Cell Response to Sendai virus infection

Project description:Oligonucleotide microarrays were used to establish a profile for gene expression in wild-type airway epithelial cells after paramyxoviral infection. Analysis was performed on mRNA isolated from SeV-infected primary-culture mouse tracheal epithelial cells that were maintained under physiologic conditions (air-liquid interface). Experiment Overall Design: Primary-culture mouse tracheal epithelial cells (mTECs) were established on Transwell membranes using air-liquid interface (ALI) conditions. Sendai virus (SeV), strain 52, was obtained from American Type Culture Collection and stored at -70Â°C. Cultures were inoculated with SeV or an equivalent amount of UV-inactivated SeV (SeV-UV) in the apical compartment for 1 h at 37 Â°C. Air-liquid-interface conditions were re-established by washing the membrane with PBS. Each culture well was subjected to one of two treatments (SeV, or UV-SeV) for 1 day. N = 4 SeV wells, N = 6 UV-SeV wells, with each well independently analyzed by microarray. No technical replicates were performed, but arrays were evaluated for quality control using the SimpleAffy package (Miller CJ, 2004) in Bioconductor 2.0.

2009-04-25 | E-GEOD-10211 | biostudies-arrayexpress

Tpl2 promotes chemokine/chemokine receptor expression and macrophage migration during acute inflammation

Project description:In autoimmune diseases, accumulation of activated leukocytes correlates with inflammation and disease progression, and therefore, disruption of leukocyte trafficking is an active area of research. The protein kinase Tpl2 (MAP3K8) regulates leukocyte inflammatory responses and is also being investigated for therapeutic inhibition during autoimmunity. Herein, we addressed the contribution of Tpl2 to the regulation of macrophage chemokine and chemokine receptor expression and subsequent migration in vivo using a mouse model of Tpl2 ablation. We found that gene expression of the chemokine ligands CCL2, CCL7, CXCL2, and CXCL3 as well as the chemokine receptors CCR1 and CCR5 were reduced in macrophages from the bone marrow and peritoneal cavities of tpl2-/- mice following stimulation with LPS. LPS stimulation repressed chemokine receptor expression of CCR1, CCR2 and CCR5. Notably, LPS-induced repression of CCR1 and CCR5 was significantly enhanced in Tpl2-deficient macrophages and was observed to be dependent upon Erk activation and independent of PI3K and mTOR signaling. Consistent with alterations in chemokine and chemokine receptor expression, tpl2-/- macrophages were defective in trafficking to the peritoneal cavity following thioglycollate-induced inflammation. Overall, this study demonstrates a Tpl2-dependent mechanism for macrophage expression of both chemokine receptors and their ligands and provides further insight into how Tpl2 inhibition may disrupt inflammatory networks in vivo. microarray was used to profile the genome-wide expression patterns in Tpl2 wild-type and deficient macrophage.

2014-06-03 | E-GEOD-48338 | biostudies-arrayexpress

Tpl2 promotes chemokine/chemokine receptor expression and macrophage migration during acute inflammation

2014-06-03 | GSE48338 | GEO

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Molecular and cellular characterization of MDSC differentiated from the bone marrow of Balb/c mice with tumor conditioned media or tumor conditioned media and antagonists for CCR1 and CCR5

Project description:Tumor derived factors can promote the differentiation of hematopoietic precursors into suppressive myeloid derived suppressor cells however, the molecular pathways that regulate this differentiation are not fully disclosed. In this study we identified a pathway by which tumor derived factors induce the expression of CCL3 and CCL4 from early HSPCs that autocrinally bind to CCR1 and CCR5 mediate the differentiation of BM cells into suppressive and protumoral cells. Inhibition of CCR1 and CCR5 is sufficient to prevent MDSC differentiation and restore the generation of myeloid cells with a tumoricidal function.

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Gene Expression Profiling Of TTLL12 Knocked Down Cell With Sendai Virus Treatment

Project description:Upon virus infection, RIG-I-like receptors in host cells recognize viral RNA and activate type I interferon expression. To investigate the role of protein methylation in the anti-viral signaling pathway, we screened all the SET domain containing proteins and identified TTLL12 as a negative regulator of RIG-I signaling pathway. TTLL12 contains SET and TTL domains, which are predicted to have lysine methyltransferase and tubulin tyrosine ligase activities, respectively. Exogenous expression of TTLL12 represses IFN-β expression induced by SeV. TTLL12 deficiency by RNA interference and CRISPR-gRNA techniques increases the induced IFN-β expression and inhibits virus replication in the cell. Gene expression profiling also indicated that TTLL12 specifically inhibits the expression of the downstream genes of innate immunity pathways. Cell fractionation and fluorescent staining indicated that TTLL12 is localized in the cytosol. The study of various mutants suggested TTLL12’s ability to repress RIG-I pathway is probably not dependent on protein modifications. Instead, TTLL12 directly interacts with VISA, TBK1 and IKKε, and inhibits the interactions of VISA with other signaling proteins. Taken together, our findings demonstrate TTLL12 as a negative regulator of RNA-virus-induced type I IFNs expression through inhibition of the interaction of VISA with other proteins.

2017-03-07 | GSE83849 | GEO

Gene expression profile of sendai virus infected primary MEFs.

Project description:To investivate the role of mitochondrial-mediate antiviral innate immunity in MEFs, we performed Sendai virus (SeV) infection experiments at the different cultured conditions of the cells. We analyzed the gene expression profile of MEFs that infected or uninfected with SeV either cultured the cells under glucose or galactose medium, and investigate its differences. We found that the both cultured conditions of cells showed normal antiviral responses.

2017-05-31 | GSE75399 | GEO

Exhausted CD8+ T cells overexpress CCL5 during combination therapy to mediate resistance of hepatoma cells to lenvatinib: one situation may contribute to the survival of residual tumor cells

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