Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE23622
PROVIDER: PRJNA133351 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mechanisms Establishing TLR4-Responsive Activation States of Inflammatory Response Genes
| PRJNA129939 | ENA
Project description:Mechanisms Establishing TLR4-Responsive Activation States of Inflammatory Response Genes (Illumina sequencing data)
| PRJNA133349 | ENA
Project description:Mechanisms Establishing TLR4-Responsive Activation States of Inflammatory Response Genes (Illumina expression data)
| PRJNA133353 | ENA
Project description:TLR4-activated immune response, elicited by exogenous or endogenous ligands, does give rise to several acute and chronic diseases, and plays a critical role as an amplifier of the inflammatory response. Along with, a cluster of TLR4-responsive miRNAs create a crosstalk during inflammatory escalation. Our data shows miR-146a even not having binding sites for different signalling mediators, alleviates pro-inflammatory response by modulating different stress-induced response (cytokine production, generation of NO, apoptosis etc) to reestablish macrophage homeostasis. We were curious to unravel this phenomenon. Here, we have reported miR-146a influences the biogenesis of a group of miRNAs after its overexpression. We have adopted a tet-on responsive miR-146a overexpression system in murine macrophages. A group of miRNAs has shown significant differential expression after miR-146a overexpression. Later, our targetome-based study correlated with this observation to establish the link between augmentations of anti-inflammatory response inside the cells with the miR-146a overexpression that probably have a significant role in establishing cellular homeostasis.
2022-02-17 | GSE172473 | GEO
Project description:Inflammatory response plays an essential role in the resolution of infections. However, inflammation can be detrimental to the organism and cause irreparable damage, for example during sepsis, when a “cytokine storm” can lead to multiple organ failure and often ends in death. One of the strongest triggers of inflammatory response is bacterial lipopolysaccharide (LPS), acting mostly through Toll-like receptor 4 (TLR4). Prior or prolonged exposure to LPS, however, can induce the state of “endotoxin tolerance” where the macrophages and monocytes do not respond to new endotoxin challenge. The cellular mechanisms regulating this phenomenon remain elusive. Our comprehensive secreted protein analysis comparing LPS-tolerant and -responsive monocyte/macrophage-like cells combined with the extracellular flux analysis reveals the robust switch from the inflammatory to metabolic protein expression as well as points to the involvement of specific proteins that may regulate the change from the responsive to the tolerant state
2021-09-09 | PXD021925 | Pride
Project description:Complete activation of macrophage proinflammatory and antimicrobial phenotype is promoted by combined action of IFN-g and LPS. Synergistic activation of canonical inflammatory NF-kB target genes by IFN-g and LPS is well appreciated, but less is known about whether IFN-g negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-g selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-g-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-g-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-g. These findings reveal that IFN-g suppresses feedback inhibitory and metabolic components of the TLR response to achieve full macrophage activation and provide insights into mechanisms by which IFN-g selectively inhibits TLR4-induced transcription.
2019-06-12 | GSE131294 | GEO
Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.
2019-06-20 | GSE130567 | GEO
Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.
2019-06-12 | GSE120944 | GEO
Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.
2019-06-12 | GSE120943 | GEO
Project description:Complete polarization of macrophages towards an M1-like proinflammatory and antimicrobial state requires combined action of IFN-γ and LPS. Synergistic activation of canonical inflammatory NF-κB target genes by IFN-γ and LPS is well appreciated, but less is known about whether IFN-γ negatively regulates components of the LPS response, and how this affects polarization. A combined transcriptomic and epigenomic approach revealed that IFN-γ selectively abrogates LPS-induced feedback and select metabolic pathways by suppressing TLR4-mediated activation of gene enhancers. In contrast to superinduction of inflammatory genes via enhancers that harbor IRF sequences and bind STAT1, IFN-γ-mediated repression targeted enhancers with STAT sequences that bound STAT3. TLR4-activated IFN-γ-suppressed enhancers comprised two subsets distinguished by differential regulation of histone acetylation and recruitment of STAT3, CDK8 and cohesin, and were functionally inactivated by IFN-γ. These findings reveal that IFN-γ suppresses feedback inhibitory and metabolic components of the TLR response to achieve full M1 polarization, and provide insights into mechanisms by which IFN-γ selectively inhibits TLR4-induced transcription.
2019-06-12 | GSE120942 | GEO