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Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE80132 | GEO | 2016/07/11

SECONDARY ACCESSION(S): PRJNA318003

REPOSITORIES: GEO

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Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation.

Project description:The host innate immune response is the first line of defense against pathogens and is orchestrated by the concerted expression of genes induced by microbial stimuli. Deregulated expression of these genes is linked to the initiation and progression of diseases associated with exacerbated inflammation. We identified topoisomerase 1 (Top1) as a positive regulator of RNA polymerase II transcriptional activity at pathogen-induced genes. Depletion or chemical inhibition of Top1 suppresses the host response against influenza and Ebola viruses as well as bacterial products. Therapeutic pharmacological inhibition of Top1 protected mice from death in experimental models of lethal inflammation. Our results indicate that Top1 inhibition could be used as therapy against life-threatening infections characterized by an acutely exacerbated immune response.

| S-EPMC5193222 | biostudies-literature

Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation (RNA-Seq)

Project description:The host innate immune response is the first line of defense against pathogens and is orchestrated by the concerted expression of genes induced by microbial stimuli. Deregulated expression of these genes is linked to the initiation and progression of numerous diseases associated with exacerbated inflammation. Here, we identify Topoisomerase 1 (Top1) as a critical positive regulator of RNA polymerase II (RNAPII) transcriptional activity at pathogen-induced genes. Notably, depletion or chemical inhibition of Top1 suppresses the host response against replicating Influenza and Ebola viruses as well as bacterial products. As a result, therapeutic pharmacological inhibition of Top1 protects mice from death in experimental models of chemical- and pathogen-induced lethal inflammation. Our results indicate that Top1 inhibition could be used as therapy against life threatening infections characterized by an acutely exacerbated immune response.

2016-07-11 | GSE80131 | GEO

Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation (ChIP-Seq)

Project description:The host innate immune response is the first line of defense against pathogens and is orchestrated by the concerted expression of genes induced by microbial stimuli. Deregulated expression of these genes is linked to the initiation and progression of numerous diseases associated with exacerbated inflammation. Here, we identify Topoisomerase 1 (Top1) as a critical positive regulator of RNA polymerase II (RNAPII) transcriptional activity at pathogen-induced genes. Notably, depletion or chemical inhibition of Top1 suppresses the host response against replicating Influenza and Ebola viruses as well as bacterial products. As a result, therapeutic pharmacological inhibition of Top1 protects mice from death in experimental models of chemical- and pathogen-induced lethal inflammation. Our results indicate that Top1 inhibition could be used as therapy against life threatening infections characterized by an acutely exacerbated immune response.

2016-07-11 | GSE80129 | GEO

Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation

Project description:Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation

| PRJNA318003 | ENA

Co-ordinate inhibition of autism candidate genes by topoisomerase inhibitors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-30 | E-GEOD-43900 | biostudies-arrayexpress

Co-ordinate inhibition of autism candidate genes by topoisomerase inhibitors

Project description:This SuperSeries is composed of the SubSeries listed below.

2013-08-30 | GSE43900 | GEO

FBXL10 Protects Polycomb-bound Genes from Hypermethylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-04-06 | E-GEOD-65583 | biostudies-arrayexpress

Inhibition of astrocytic DRD2 suppresses CNS inflammation in an animal model of multiple sclerosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-15 | GSE205292 | GEO

Topoisomerase II inhibition involves characteristic chromosomal expression patterns

Project description:This SuperSeries is composed of the SubSeries listed below.

2008-10-01 | GSE11942 | GEO

Inhibition of RIPK3 Pathway Attenuates Intestinal Inflammation and Cell Death of Inflammatory Bowel Disease and Suppresses Necroptosis in Peripheral Mononuclear Cells of Ulcerative Colitis Patients.

Project description:Receptor-interacting serine/threonine-protein kinase (RIPK) 3 is a member of the TNF receptor-I signaling complex and mediates necroptosis, an inflammatory cell death. Ulcerative colitis (UC) is an excessive inflammatory disease caused by uncontrolled T cell activation. The current study is aimed to determine whether RIPK3 inhibitor attenuates UC development inhibiting inflammation and necroptosis using experimental colitis mice model. Dextran sulfate sodium-induced colitis mice were administered RIPK3 inhibitor (3 mg/ml) 3 times and their tissues were analyzed by immunohistochemistry. RIPK3, mixed lineage kinase domain-like (MLKL), phosphorylated MLKL, IL-17, and CD4 in colitis patient colon tissues were detected using confocal microscopy. Protein levels were measured using immunohistochemistry and ELISA. The differentiation of Th17 cells was evaluated using flow cytometry. The expression of proinflammatory cytokines and necroptosis in peripheral blood mononuclear cells from UC patients was decreased markedly by RIPK3 inhibitor treatment. We also observed that the injection of RIPK3 inhibitor improves colitis severity and protects intestinal destruction. RIPK3 inhibitor reduced necroptosis factors and proinflammatory cytokines in the colon and consequently protected colon devastation. The expression of inflammatory mediators in experimental colitis mice splenocytes was decreased significantly by RIPK3 inhibitor treatment. These results suggest that RIPK3 inhibitor ameliorates severity of experimental colitis and reduces inflammation through the inhibition of inflammatory response and necroptosis and support RIPK3-targeting substances for treatment of UC.

| S-EPMC7192830 | biostudies-literature

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