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Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

ABSTRACT: comparing different lineages of M.tb strains (lineages 3 and 4) in interrupting of epithelial signalling pathways in A549 cell line, from TLRs and NFkB signalling pathways to specific cytokine secretion

ORGANISM(S): Homo sapiens

PROVIDER: GSE112998 | GEO | 2018/04/13

REPOSITORIES: GEO

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Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

Project description:comparing different lineages of M.tb strains (lineages 3 and 4) in interrupting of epithelial signalling pathways in A549 cell line, from TLRs and NFkB signalling pathways to specific cytokine secretion

2018-04-13 | GSE113050 | GEO

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains

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

2018-04-13 | GSE113051 | GEO

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

Project description:Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [NFkB]

| PRJNA449901 | ENA

Classical and/or alternative NF-kB pathway activation in multiple myeloma pathogenesis

Project description:Mutations involving the NFKB pathway are present in at least 17% of multiple myeloma (MM) tumors and 40% of MM cell lines (MMCL). These mutations, which are thought to be progression events, enable MM tumors to become less dependent on extrinsic bone marrow signals that activate NFKB. Studies on a panel of 50 MMCL provide some clarification of the mechanisms through which these mutations act and the significance of classical vs alternative activation of NFKB. First, only one mutation (NFKB2) selectively activates the alternative pathway, whereas several mutations (CYLD, NFKB1, TACI) selectively activate the classical pathway. However, most mutations affecting NIK level (NIK, TRAF2, TRAF3, cIAP1&2, CD40) activate the alternative but often both pathways. Second, we confirm the critical role of TRAF2 in regulating NIK degradation, whereas TRAF3 enhances but is not essential for cIAP1/2-mediated proteosomal degradation of NIK in MM. Third, using transfection to selectively activate the classical or alternative NFKB pathways, we show virtually identical changes in gene expression in one MMCL, whereas the changes are similar albeit non-identical in a second MMCL. Together, our results suggest that MM tumors can achieve increased autonomy from the bone marrow microenvironment by mutations that activate either NFKB pathway.

2009-09-11 | GSE18047 | GEO

Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

Project description:Comparative study of interruption of TLR and NF-kB signaling pathways in lung epithelial cell by Mycobacterium tuberculosis strains [TLR]

| PRJNA449900 | ENA

Mitochondrial outer membrane integrity regulates a ubiquitin-dependent NF-kB inflammatory response

Project description:Mitochondria are often essential for apoptosis through mitochondrial outer membrane permeabilization (MOMP). This central event enables cytochrome c release leading to caspase activation and rapid cell death. Recently, MOMP has been shown to be inherently pro-inflammatory, for instance, causing mitochondrial DNA-dependent activation of cGAS-STING signalling. Alongside having emerging functions in health and disease, MOMP associated inflammation can also elicit anti-tumour immunity. Nonetheless, how MOMP triggers inflammation and how the cell counteracts this remain poorly defined. Here, we find that upon MOMP, mitochondria are ubiquitylated in a promiscuous manner targeting proteins localised to both inner and outer mitochondrial membranes. Mitochondrial ubiquitylation serves to recruit the essential adaptor molecule, NEMO, leading to activation of pro-inflammatory NF-kB signalling. We find that disruption of mitochondrial outer membrane integrity through different means leads to engagement of a similar pro-inflammatory signalling platform. Thus, mitochondrial integrity directly controls inflammation, whereby permeabilised mitochondria initiate NF-?B signalling. This may be important for the various pathophysiological functions of MOMP-associated inflammation.

2023-12-15 | PXD040192 | Pride

CRISPR/Cas9-mediated Gene Knockout Reveals a Guardian Role of NF-kB/RelA in Maintaining the Homeostasis of Human Vascular Cells

Project description:Dysfunction of blood vessels leads to severe vasculature pathogenesis. Previous studies have demonstrated that constitutive NFkB activation results in chronic vascular inflammation, leading to various cardiovascular diseases. However, how NFkB regulates blood vessel homeostasis remains largely elusive. Here, using CRISPR/Cas9-mediated gene editing, we generated RelA knockout human embryonic stem cells (hESCs) and differentiated them into human vascular derivatives to study how NFkB modulates vascular cells under basal and inflammatory conditions. Multi-dimensional phenotypic assessments and transcriptomic analyses revealed that RelA deficiency affected vascular cells via modulating vascular inflammation, survival, vasculogenesis, differentiation and extracellular matrix organization in a cell type-specific manner under basal condition, and that RelA protected vascular cells against apoptosis and modulated vascular inflammatory response upon TNFa stimuli. Lastly, further evaluation of gene expression patterns in IkBa knockout vascular cells demonstrated that IkBa acted largely independent of NFkB signaling pathway. Taken together, our data reveals a protective role of NFkB/RelA in modulating human blood vessel homeostasis and maps the human vascular transcriptomic landscapes for the discovery of novel therapeutic targets.

2018-06-05 | GSE115311 | GEO

NF-kB regulator Bcl3 modulates bone density and turnover

Project description:B-cell lymphoma 3-encoded protein (Bcl3) is an intimate and context-specific regulator of the NF-kB family of transcription factors, a ubiquitous master regulator involved in many homeostatic and inflammatory processes. NF‑kB signalling determines the fates of bone-forming osteoblasts and bone-resorbing osteoclasts. Herein we show that Bcl3 is a negative regulator of NF‑kB via control of osteoblast and osteoclast function. Mice lacking Bcl3 (Bcl3−/−) have congenitally increased bone density, long bone dwarfism, increased biomechanical strength and altered bone turnover. Bcl3−/− osteoblasts and osteoclasts have accelerated differentiation and increased activity; whereas, rescue overexpression with a Bcl3 mimetic peptide inhibits differentiation. Early-differentiating Bcl3−/− osteoblasts have altered gene transcription favouring bone formation, including perturbation of the RANKL-OPG axis. In a model of osteoarthritic aberrant mineralisation Bcl3−/− mice exhibit decreased pathological osteophyte formation. Cumulatively, these findings identify Bcl3 as a viable target for controlling NF‑kB signalling in the treatment of skeletal pathologies.

2019-01-17 | GSE125153 | GEO

Expression of TLR-7, MyD88, NF-kB, and INF-? in B Lymphocytes of Mayan Women with Systemic Lupus Erythematosus in Mexico.

Project description:BackgroundSystemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease involving multiple organs. It is currently accepted that several genetic, environmental, and hormonal factors are contributing to its development. Innate immunity may have a great influence in autoimmunity through Toll-like receptors. TLR-7 recognizing single-strand RNA has been involved in SLE. Its activation induces intracellular signal with attraction of MyD88 and NF-kBp65, leading to IFN-? synthesis which correlate with disease activity.ObjectiveTo assess the expression of TLR-7, MyD88, and NF-kBp65 in B lymphocytes of Mayan women with SLE.MethodsOne hundred patients with SLE and 100 healthy controls, all of them Mayan women, were included. TLR-7 was analyzed on B and T lymphocytes, and MyD88 and NF-kB only in B lymphocytes. Serum INF-? level was evaluated by ELISA.ResultsSignificant expression (p?<?0.0001) of TLR-7 in B and T lymphocytes and serum IFN-? increased (p?=?0.034) was observed in patients. MyD88 and NF-kBp65 were also increased in B lymphocytes of patients. TLR-7 and NF-kBp65 expression correlated, but no correlation with INF-? and disease activity was detected.ConclusionData support the role of TLR-7 and signal proteins in the pathogenesis of SLE in the Mayan population of Yucatán.

| S-EPMC4735402 | biostudies-literature

Severity of DSS-induced colitis is reduced in Ido1-deficient mice with down-regulation of TLR-MyD88-NF-kB transcriptional networks.

Project description:Indoleamine 2,3 -dioxygenase 1 (IDO1) catalyzes L-tryptophan to kynurenine in the first and rate-limiting step of tryptophan metabolism. IDO1 is expressed widely throughout the body, with especially high expression in colonic intestinal tissues. To examine the role of IDO1 in the colon, transcriptome analysis was performed in both Ido1(-/-) and Ido1(+/+) mice. Gene set enrichment analysis identified the Inflammatory Response as the most significant category modulated by the absence of IDO1. This observation prompted us to further investigate the function of IDO1 in the development of tissue inflammation. By using DSS-induced experimental colitis mice models, we found that the disease in Ido1(-/-) mice was less severe than in Ido1(+/+) mice. Pharmacological inhibition of IDO1 by L-1MT attenuated the severity of DSS-colitis as well. Transcriptome analyses revealed that pathways involving TLR and NF-kB signaling were significantly down-regulated by the absence of IDO1. Furthermore, dramatic changes in TLR and NF-kB signaling resulted in substantial changes in the expression of many inflammatory cytokines and chemokines. Numbers of inflammatory cells in colon and peripheral blood were reduced in IDO1 deficiency. These findings suggest that IDO1 plays important roles in producing inflammatory responses and modulating transcriptional networks during the development of colitis.

| S-EPMC4661522 | biostudies-literature

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