IκBζ-dependent responses in keratinocytes upon Staphylococcus aureus infection
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ABSTRACT:
PROVIDER: PRJNA1112376 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29057715_1.fastq.gz | Fastqsanger.gz | |||
| SRR29057715_2.fastq.gz | Fastqsanger.gz | |||
| SRR29057716_1.fastq.gz | Fastqsanger.gz | |||
| SRR29057716_2.fastq.gz | Fastqsanger.gz | |||
| SRR29057717_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study we investigated the transcriptional responses of keratinocyte-derived IκBζ (encoded by NFKBIZ) upon infection with the pathogenic Staphylococcus aureus (S. aureus) USA300 wildtype strain.
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Project description:HIF-1 is an important transcription factor for immune responses to bacterial infection. We wanted to analyze the HIF-1 dependent gene expression upon S. aureus infection and analyzed the gene expression of HepG2 nt and HepG2 HIF-1-/- cells four hours upon infection using affymetrix human gene 1.0 st. gene arrays. triplicates of HepG2 nt and HepG2 HIF-1-/- cells were infected with S. aureus 8325-4 (4 h, MOI: 20), triplicates of uninfected cells were used as control
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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
Project description:HIF-1 is an important transcription factor for immune responses to bacterial infection. We wanted to analyze the HIF-1 dependent gene expression upon S. aureus infection and analyzed the gene expression of HepG2 nt and HepG2 HIF-1-/- cells four hours upon infection using affymetrix human gene 1.0 st. gene arrays.
2013-08-01 | GSE44943 | GEO
Project description:Background: IκBζ, a rather unknown co-regulator of NF-κB, is mostly inducibly expressed and can either activate or repress a specific subset of NF-κB target genes. While its role as a transcriptional regulator of various cytokines and chemokines in immune cells has been revealed, IκBζ’s function in solid cancer remains unclear. Methods: We investigated IκBζ expression in melanoma, and assessed its impact on target gene expression, tumor growth, and response to immunotherapy in melanoma cell lines, mouse models, and patient samples. Results: Unlike in other cell types, IκBζ protein was found to be constitutively expressed in a subfraction of melanoma cell lines, and around 35% of melanoma cases. This atypical expression pattern of IκBζ did not correlate with its mRNA levels or known driver mutations, but instead seemed to result from changes in its post-transcriptional or post-translational regulation. Deleting constitutively expressed IκBζ abrogated the activity and chromatin association of STAT3 and p65, leading to reduced expression of the pro-proliferative cytokines IL-1β and IL-6 in melanoma cells. Consequently, loss of tumor-derived IκBζ suppressed self-sustained melanoma cell growth both in vitro and in vivo. Additionally, constitutive IκBζ expression suppressed the induction of the chemokines CXCL9, CXCL10, and CCL5, which impaired the recruitment of NK and CD8+ T-cells to the tumor, causing resistance to α-PD-1 immunotherapy in mice. Furthermore, the expression of tumor-derived IκBζ also correlated with the absence of CD8+ T-cells in human melanoma samples and progressive disease during immunotherapy. Conclusion: We propose that tumor-derived IκBζ could serve as a new therapeutic target and prognostic marker that characterizes melanoma with high tumor cell proliferation, cytotoxic T- and NK-cell exclusion, and unfavorable immunotherapy responses. Targeting IκBζ expression might open up a new therapy option to re-establish the recruitment of cytotoxic cells, thereby resensitizing for immunotherapy.
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Project description:Background: IκBζ, a rather unknown co-regulator of NF-κB, is mostly inducibly expressed and can either activate or repress a specific subset of NF-κB target genes. While its role as a transcriptional regulator of various cytokines and chemokines in immune cells has been revealed, IκBζ’s function in solid cancer remains unclear. Methods: We investigated IκBζ expression in melanoma, and assessed its impact on target gene expression, tumor growth, and response to immunotherapy in melanoma cell lines, mouse models, and patient samples. Results: Unlike in other cell types, IκBζ protein was found to be constitutively expressed in a subfraction of melanoma cell lines, and around 35% of melanoma cases. This atypical expression pattern of IκBζ did not correlate with its mRNA levels or known driver mutations, but instead seemed to result from changes in its post-transcriptional or post-translational regulation. Deleting constitutively expressed IκBζ abrogated the activity and chromatin association of STAT3 and p65, leading to reduced expression of the pro-proliferative cytokines IL-1β and IL-6 in melanoma cells. Consequently, loss of tumor-derived IκBζ suppressed self-sustained melanoma cell growth both in vitro and in vivo. Additionally, constitutive IκBζ expression suppressed the induction of the chemokines CXCL9, CXCL10, and CCL5, which impaired the recruitment of NK and CD8+ T-cells to the tumor, causing resistance to α-PD-1 immunotherapy in mice. Furthermore, the expression of tumor-derived IκBζ also correlated with the absence of CD8+ T-cells in human melanoma samples and progressive disease during immunotherapy. Conclusion: We propose that tumor-derived IκBζ could serve as a new therapeutic target and prognostic marker that characterizes melanoma with high tumor cell proliferation, cytotoxic T- and NK-cell exclusion, and unfavorable immunotherapy responses. Targeting IκBζ expression might open up a new therapy option to re-establish the recruitment of cytotoxic cells, thereby resensitizing for immunotherapy.
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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
Project description:Interactions between human keratinocytes and secreted factors from Staphylococcus aureus biofilm were investigated using microarray analysis. Relative to control cells, biofilm-secreted factors upregulated cytokine and chemokine genes in keratinocytes. Genes associated with DNA damage and oxidative stress were also induced in keratinocytes treated with secreted factors from S. aureus. Here we show that secreted factors from S. aureus biofilm cultures differentially impact several aspects of wound healing processes. Human keratinocytes were grown in co-culture with mature S. aureus biofilms for 24 hours. Keratinocytes exposed to S. aureus biofilm were analyzed in quadruplicate. Control cells were also analyzed in quadruplicate. Dye-swaps were performed.
2011-08-30 | E-GEOD-24370 | biostudies-arrayexpress
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.
2013-04-09 | GSE43075 | GEO