Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcriptome analysis in macrophages treated with type I interferon, heat-killed Listeria monocytogenes, or both.

ABSTRACT: To define the group of genes which is synergistically induced by cooperative activity of the type I interferon - activated Jak/STAT pathway and other pathways, we treated bone marrow-derived macrophages (BMDM) with heat-killed Listeria (hkL; non-STAT pathways activated), type I interferon alone (only STAT pathway activated), or both stimuli together.

ORGANISM(S): Mus musculus

SUBMITTER: Sebastian Wienerroither

PROVIDER: E-MTAB-3015 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-κB Pathways by Concerted Recruitment of the Mediator Complex.

Wienerroither Sebastian S Shukla Priyank P Farlik Matthias M Majoros Andrea A Stych Bernadette B Vogl Claus C Cheon HyeonJoo H Stark George R GR Strobl Birgit B Müller Mathias M Decker Thomas T

Cell reports 20150702 2

The transcriptional response to infection with the bacterium Listeria monocytogenes (Lm) requires cooperative signals of the type I interferon (IFN-I)-stimulated JAK-STAT and proinflammatory NF-κB pathways. Using ChIP-seq analysis, we define genes induced in Lm-infected macrophages through synergistic transcriptional activation by NF-κB and the IFN-I-activated transcription factor ISGF3. Using the Nos2 and IL6 genes as prime examples of this group, we show that NF-κB functions to recruit enzymes ...[more]

PMID: 26146080

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Project description:Exciting discoveries related to IL-1R/TLR signaling in development of atherosclerosis plaque have triggered intense interest in the molecular mechanisms by which innate immune signaling modulates the onset and development of atherosclerosis. Previous studies have clearly shown the definitive role of proinflammatory cytokine IL-1 in the development of atherosclerosis. Recent studies have provided direct evidence supporting a link between innate immunity and atherogenesis. While it is still controversial about whether infectious pathogens contribute to cardiovascular diseases, direct genetic evidence indicates the importance of IL-1R/TLR signaling in atherogenesis. In this study, we examined the role of IRAK4 kinase activity in modified LDL-mediated signaling using bone marrow-derived macrophage as well as in vivo model of atherosclerosis. First, we found that the IRAK4 kinase activity was required for modified LDL-induced NFÎºB activation and expression of a subset of proinflammatory genes, but not for the activation of MAPKs in bonemarrow-derived macrophage. IRAK4 kinase inactive knock-in (IRAK4KI) mice were bred onto ApoE-/- mice to generate IRAK4KI/ApoE-/- mice. Importantly, the aortic sinus lesion formation was impaired in IRAK4KI/ApoE-/- mice compared to that in ApoE-/- mice. Furthermore, proinflammatory cytokine production was reduced in the aortic sinus region of IRAK4KI/ApoE-/- mice compared to that in ApoE-/- mice. Taken together, our results indicate that the IRAK4 kinase plays an important role in modified LDL-mediated signaling and the development of atherosclerosis, suggesting that pharmacological inhibition of IRAK4 kinase activity might be a feasible approach in the development of anti-atherosclerosis drugs. To identify global changes in gene expression, we examined gene expression profiles of macrophages from wild-type and IRAK4 kinase-inactive knock-in mice in response to acLDL stimulation using the Illumina microarray with probes for 23,000 transcripts. Bone marrow-derived macrophages from wild-type and IRAK4 kinase-inactive knock-in mice were treated with acLDL for 24 hours.

Dataset Information

Transcriptome analysis in macrophages treated with type I interferon, heat-killed Listeria monocytogenes, or both.

Publications

Cooperative Transcriptional Activation of Antimicrobial Genes by STAT and NF-κB Pathways by Concerted Recruitment of the Mediator Complex.

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