Evaluation of induced cellular cytokine profile in response to Rifampin-mono resistant Mycobacterium tuberculosis strain
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PROVIDER: PRJNA475416 | ENA |
REPOSITORIES: ENA
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Project description:Comparing of induced cellular cytokine profile in response to Rifampin-mono resistant and H37Rv Mycobacterium tuberculosis strains
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Project description:Engineering CAR T cells expressing specific chimeric cytokine receptors that signal independently from the presence of an exogenous cytokine can significantly impact cancer cellular therapy by improving : i) trafficking and expansion of the adoptive cells therapy product post-infusion, ii) extended persistence of the modified T cells post tumour eradication. Altogether, these features will allow lifelong tumour protection. Furthermore, the technology here illustrated holds the potential to reduce the dose required to reach therapeutic efficacy, greatly reducing the overall manufacturing cost. Finally, the generalisability of the architecture described holds the potential to tailor a specific cytokine signal to a particular type of cell that the developed therapy is based upon.
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Project description:Bisphenol S and mono-ethylhexyl phthalate are widely used in the industry of making plastic, mailing envelopes, tickets, etc. Humans are exposed to these compounds by skin contact, inhalation, and food ingestions. However, the molecular mechanisms of these compounds' adverse effects are still unclear. We address the molecular and cellular mechanisms underlying Bisphenol S and mono-ethylhexyl phthalate effects on HeLa cells. Here microarray analysis was performed to identify distinct classes of up- or down-regulated genes and their connections to the different metabolic pathways.
2020-05-27 | GSE147533 | GEO
Project description:Organotypic three dimensional cultures of epithelial cells are grown at the air–liquid interface (ALI) and resemble the in vivo counterparts. Although the complexity of in vivo cellular responses could be better manifested in co-culture models in which additional cell-types such as fibroblasts were incorporated, the presence of another cell-type could mask the response of the other. This study reports the impact of whole combustible cigarette smoke (CS) on organotypic mono- and co-culture models to evaluate the relevancy of organotypic models for toxicological assessment of aerosols. Two organotypic bronchial models were directly exposed to low and high concentrations of CS of the reference research cigarette 3R4F: mono-culture of bronchial epithelial cells without fibroblasts (BR) and co-culture with fibroblasts (BRF) models. Adenylate kinase-based cytotoxicity, cytochrome P450 (CYP) 1A1/1B1 activity, tissue histology, and concentrations of secreted mediators in the basolateral media, as well as transcriptomes were evaluated following the CS exposure. The results demonstrated similar impact of CS on the AK-based cytotoxicity, CYP1A1/1B1 activity, and tissue histology in both models. However, a greater number of secreted mediators were found in the basolateral media of the mono-culture than in the co-culture models. Furthermore, annotation analysis and network-based systems biology analysis of the transcriptomic profiles indicated a more prominent cellular stress and tissue damage following CS in the mono-culture epithelium model without fibroblasts. Finally, our results indicated that the in vivo smoking-induced xenobiotic metabolism response in the bronchial epithelial cells was better reflected on the in vitro co-culture model upon CS exposure.
2015-06-12 | E-MTAB-3462 | biostudies-arrayexpress
Project description:In an inducible model of human breast cellular transformation, we map genome-wide chromatin binding of S100A8, S100A9 and Pol II. We show that the calcium-dependent cytokines S100A8 and S100A9 are recruited to numerous promoters and enhancers. This recruitment is associated with multiple DNA sequence motifs recognized by DNA-binding transcription factors that are linked to transcriptional activation and are important for transformation. Nuclear-specific expression of S100A8/A9 promotes oncogenic transcription and leads to enhanced breast transformation phenotype. These results suggest that, in addition to its classical cytokine function, S100A8/A9 can act as a transcriptional co-activator.
2021-01-01 | GSE155421 | GEO
Project description:Pancreatic beta-cells are essential for survival, being the only cell type capable of insulin secretion. While they are believed to be vulnerable to damage by inflammatory cytokines such as interleukin-1 beta (IL-1beta) and IFN-gamma, we have recently identified physiological roles for cytokine signaling in rodent beta-cells that include that stimulation of antiviral and antimicrobial gene expression and the inhibition of viral replication. In this study, we examine cytokine-stimulated changes in gene expression in human islets using single-cell RNA sequencing. Surprisingly, the global responses of human islets to cytokine exposure were remarkably blunted compared to our previous observations in the mouse. The small population of human islet cells that were cytokine responsive exhibited increased expression of IL-1beta-stimulated antiviral guanylate binding proteins, just like in the mouse. Most human islet cells were not responsive to cytokines, and this lack of responsiveness was associated with high expression of genes encoding ribosomal proteins. We further correlated the expression levels of RPL5 with stress response genes, and when expressed at high levels, RPL5 is predictive of failure to respond to cytokines in all endocrine cells. Further, we postulate that donor cause of death and isolation methodologies may contribute to stress of the islet preparation. Our findings indicate that induction of stress responses in human islets (associated with isolation and/or cause of death) limit cytokine stimulated gene expression, and we urge caution in the evaluation of studies that have examined cytokine-stimulated gene expression in human islets without evaluation of stress-related gene expression.
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Project description:Transcriptional profiling of K. vulgare cells co-cultured with Bacillus megaterium compared to K. vulgare mono-cultured cells. Differentially expressed genes in co-cultured and mono-cultured K. vulgare cells were analyzed. The aim was to investigate the mechanisms of B. megaterium stimulating K. vulgare propagation on global gene expression. Two-condition experiment: co-cultured K. vulgare and B. megaterium cells vs. mono-cultured K. vulgare cells. Biological replicates: 3 co-cultured replicates, 3 mono-cultured replicates.
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Project description:Understanding the mechanisms underlying the acquisition and maintenance of effector function during T cell differentiation is important to unraveling how these processes can be dysregulated in the context of disease and manipulated for therapeutic intervention. Herein, we report the identification of a novel regulator of murine T cell differentiation through the evaluation of a previously unreported activity of the kinase inhibitor, BioE-1197. Specifically, we demonstrate liver kinase B1 (LKB1) mediated activation of salt-inducible kinases (SIKs) epigenetically regulates cytokine recall potential in effector CD8+ and Th1 cells. Evaluation of this phenotype revealed SIK mediated phosphorylation dependent stabilization of histone deacetylase 7 (HDAC7) occurred during late-stage effector differentiation. HDAC7 stabilization increased nuclear HDAC7 levels which correlated with both global and cytokine loci specific reductions in the activating transcription mark, histone 3 lysine 27 acetylation (H3K27Ac). Accordingly, HDAC7 stabilization diminished transcriptional induction of cytokine upon re-stimulation. Inhibition of this pathway during differentiation produced effector T cells epigenetically poised for enhanced cytokine recall. This work identifies a novel target for enhancing effector T cell functionality.
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