Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

IκBζ-deficient epidermis mediates systemic autoimmune inflammation via skin dysbiosis.

ABSTRACT: Skin microbiota affect systemic inflammation through mechanisms that have not been completely elucidated. We previously demonstrated that keratinocyte-specific IκBζ-deficient mice spontaneously develop autoimmune inflammation resembling human Sjögren syndrome. In this study, we examined how IκBζ-deficient epidermis dictates systemic autoimmune inflammation onset. To examine if IκBζ-deficient keratinocytes are susceptible to apoptotic stimuli in a steady state, we performed microarray analysis of untreated murine back epidermis. Data indicate that IκBζ-deficient epidermis is susceptible to environment antigens through apoptosis-related gene upregulation

ORGANISM(S): Mus musculus

PROVIDER: GSE165515 | GEO | 2022/08/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Inhibitor of NFκB ζ (IκBζ) is a transcriptional key regulator of monocyte chemoattractant protein-1 (MCP-1/CCL2)

Project description:Monocyte chemoattractant protein 1 (MCP-1/CCL2) is critically involved in directing the migration of blood monocytes to sites of inflammation. Consequently, excessive MCP-1 secretion has been linked to many (auto)inflammatory diseases, whereas a lack of expression severely impairs immune responsiveness. We demonstrate that the atypical inhibitor of NF-κB ζ (IκBζ), a transcriptional co-activator required for the selective expression of a subset of NF-κB target genes, is a key activator of the Ccl2 gene. IκBζ-deficient macrophages exhibited impaired secretion of MCP-1 when challenged with diverse inflammatory stimuli, such as lipopolysaccharide or peptidoglycan. These findings were reflected at the level of Ccl2 gene expression, which was tightly coupled to the presence of IκBζ. Moreover, mechanistic insights acquired by chromatin immunoprecipitation demonstrate that IκBζ is directly recruited to the proximal promoter region of the Ccl2 gene and required for histone H3K9 trimethylation. Finally, IκBζ-deficient mice showed significantly impaired MCP-1 secretion and monocyte infiltration in an experimental model of peritonitis. Together, these findings suggest a distinguished role of IκBζ in mediating the targeted recruitment of monocytes in response to local inflammatory events. Peritoneal macrophages from Wildtype and IκBζ-Knockout mice were either stimulated with 1µg/ml LPS for 4h or left untreated (triplicates each)

2013-04-09 | E-GEOD-43075 | biostudies-arrayexpress

Inhibitor of NFκB ζ (IκBζ) is a transcriptional key regulator of monocyte chemoattractant protein-1 (MCP-1/CCL2)

2013-04-09 | GSE43075 | GEO

IκBζ Regulates the Development of Nonalcoholic Fatty Liver Disease through the Attenuation of Hepatic Steatosis in Mice

Project description:IκBζ is a transcriptional regulator that augments inflammatory responses from the Toll-like receptor or interleukin signaling. These innate immune responses contribute to the progression of nonalcoholic fatty liver disease (NAFLD); however, the role of IκBζ in the pathogenesis of NAFLD remains elusive. We investigated whether IκBζ was involved in the progression of NAFLD in mice. We generated hepatocyte-specific IκBζ-deficient mice (Alb-Cre; Nfkbizfl/fl) by crossing Nfkbizfl/fl mice with Alb-Cre transgenic mice. NAFLD was induced by feeding the mice a choline-deﬁcient, L-amino acid-deﬁned, high-fat diet (CDAHFD). CDAHFD-induced IκBζ expression in the liver was observed in Nfkbizfl/fl mice, but not in Alb-Cre; Nfkbizfl/fl mice. Contrary to our initial expectation, IκBζ deletion in hepatocytes accelerated the progression of NAFLD after CDAHFD treatment. Although the increased expression of inflammatory cytokines and apoptosis-related proteins by CDAHFD remained unchanged between Nfkbizfl/fl and Alb-Cre; Nfkbizfl/fl mice, early-stage steatosis of the liver was significantly augmented in Alb-Cre; Nfkbizfl/fl mice. Overexpression of IκBζ in hepatocytes via the adeno-associated virus vector attenuated liver steatosis caused by the CDAHFD in wild-type C57BL/6 mice. This preventive effect of IκBζ overexpression on steatosis was not observed without transcriptional activity. Microarray analysis revealed a correlation between IκBζ expression and the changes of factors related to triglyceride biosynthesis and lipoprotein uptake. Our data suggest that hepatic IκBζ attenuates the progression of NAFLD possibly through the regulation of the factors related to triglyceride metabolism.

2022-06-05 | GSE205390 | GEO

Transcription profiling of minor salivary glands to identify distinct patterns of gene expression in patients with primary Sj¸gren?s syndrome (pSS), a frequent and prototype systemic autoimmune disease

Project description:Analysis of targets organs might help to get new insights into the pathogenesis of autoimmune diseases. We used global gene expression profiling of minor salivary glands to identify distinct patterns of gene expression in patients with primary Sjögrens syndrome (pSS), a frequent and prototype systemic autoimmune disease. Gene expression signature allowed to distinguish most patients with pSS from healthy controls

2005-10-01 | E-MEXP-419 | biostudies-arrayexpress

Neisseria meningitidis elicits a pro-inflammatory response involving IκBζ in a human blood-cerebrospinal fluid barrier model.

Project description:The human-specific, Gram-negative bacterium Neisseria meningitidis (Nm) is a leading cause of bacterial meningitis world-wide. It has been described that Nm can enter the central nervous system via the blood-cerebrospinal fluid barrier (BCSFB), which is constituted by the epithelial cells of the choroid plexus. Using a recently established in vitro model of the human BCSFB based on human malignant choroid plexus papilloma (HIBCPP) cells we investigated the cellular response of HIBCPP cells challenged with the meningitis-causing Nm strain MC58. In comparison we analysed the answer to the closely related unencapsulated carrier isolate Nm α14. Transcriptome analysis revealed a stronger transcriptional response after infection with strain MC58, in particular with its capsule deficient mutant MC58siaD-, which correlated with bacterial invasion levels. Expression evaluation and Gene Set Enrichment Analysis pointed to a NF-κB-mediated pro-inflammatory immune response involving up-regulation of the transcription factor IκBζ. Consistent with this, infected cells secreted significant levels of pro-inflammatory chemokines and cytokines, among others, IL8, CXCL1-3 and the IκBζ target gene product IL6. Expression profile of pattern recognition receptors in HIBCPP cells and the response to specific agonists indicates that TLR2 rather than TLR4 is involved in the cellular reaction following Nm infection.

2014-09-16 | GSE42870 | GEO

Identification of multiple transferrin species in spleen from mice with collagen-induced arthritis which may reflect changes in transferrin glycosylation associated with the disease activity. Role of CD38. Set 2 of identified proteins (MALDI TOF/TOF UltrafleXtreme, Bruker).

Project description:Collagen type II-induced arthritis (CIA) is an autoimmune disease that is accompanied by a complex host systemic response, which includes inflammatory and autoimmune reactions. Since to develop CIA is required the injection of antigen in complete Freund’s adjuvant (CFA), which is a water-in-mineral-oil emulsion containing killed Mycobacteria, systemic response proteins related with inflammation can confound the detection or diagnosis of arthritis. CIA in CD38 deficient mice (CD38 KO) is milder than that in C57BL/6 (B6 WT) mice. Protein extracts from spleen were subjected to 2D-DiGE and MS-MALDI-TOF/TOF analysis to identify proteins that were differentially expressed in CD38 KO and B6 WT mice with arthritis, with inflammation, or non-immunized. Differential protein expression was validated by ELISA, or Western-blotting.

2015-12-10 | PXD002643 | Pride

2015-12-11 | PXD003183 | Pride

2015-12-10 | PXD002644 | Pride

Human - plasma extracellular vesicles from pSS patients, SLE patients and HD

Project description:Proteomic analysis of plasma extracellular vesicles from primary Sjögren syndrom patients, compared to systemic lupus erythematosus patients and helathy donors

2023-06-13 | PXD041452 | Pride

The female-biased factor VGLL3 drives cutaneous and systemic autoimmunity: RNA-seq analysis of the K5-Vgll3 transgenic mouse model of cutaneous and systemic lupus

Project description:RNA-seq analysis of nonlesional skin, whole blood, and cultured primary keratinocytes of wild-type and autoimmunity-prone K5-Vgll3 mice, which overexpress the female-biased transcription cofactor VGLL3 in the epidermis and develop a progressive lupus-like rash and systemic autoimmune disease with features of systemic lupus erythematosus. These skin and blood data demonstrate that skin-directed overexpression of VGLL3 results in gene expression changes strikingly similar to those seen in skin and blood of patients with cutaneous and systemic lupus, respectively.

2019-03-19 | GSE128453 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data