Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA323726 | ENA |
REPOSITORIES: ENA
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Project description:To directly test whether inhibition of IL-18 by IL-18 neutralizing monoclonal antibodies (IL-18 nAbs) is sufficient for blocking the inflammatory responses of heart caused by acute β-adrenergic insult, mice were subjected to intraperitoneal injection with rat IL-18 nAbs or IgG as a negative control 1hr after isoproterenol treatment.
2016-05-31 | GSE82034 | GEO
Project description:To further search for potential gene targets which are involved in the pathological process of myocardial infarction, we have employed whole genome microarray expression profiling as a discovery platform to identify the expression of STAT6, β1-adrenergic receptors and inflammatory cytokines. The CD11b+ cells were isolated from spleen and bone marrow of mice by magnetic beads, and the experimental mice were divided into four time points (control, MI 1week, MI 2 weeks, and MI 4 weeks). We found the β1-AR related sympathetic signal, the STAT6 signal and inflammatory cytokines (IL-1α, IL-18 and TGF-β) are involved in the activation of CD11b+ immune cells and cardiac fibrogenesis after myocardial infarction.
2020-11-16 | GSE154733 | GEO
Project description:In immunosurveillance, bone-derived immune cells infiltrate the tumor and secrete inflammatory cytokines to destroy cancer cells. However, cancer cells have evolved mechanisms to usurp inflammatory cytokines to promote tumor progression. In particular, the inflammatory cytokine, interleukin-1 (IL-1), is elevated in prostate cancer (PCa) patient tissue and serum and promotes PCa bone metastasis. IL-1 also represses androgen receptor (AR) accumulation and activity in PCa cells, yet the cells remain viable; suggesting that IL-1 may also contribute to AR-targeted therapy resistance. Furthermore, IL-1 and AR protein levels negatively correlate in PCa tumor cells. Taken together, we hypothesize that IL-1 reprograms AR positive (AR+) PCa cells into AR negative (AR-) PCa cells that co-opt IL-1 signaling to ensure AR-independent survival in the inflammatory tumor microenvironment. Thus, we employed RNA sequencing to identify pathways that are modulated by IL-1 concomitant with IL-1-induced AR repression in PCa cells. Comparative analysis of sequencing data from the AR+ LNCaP PCa cell line versus the AR- PC3 PCa cell line reveals an IL-1-conferred gene suite in LNCaP cells that is constitutive in PC3 cells, and includes AR and AR target gene repression and the induction of prosurvival, lineage, and cancer stem cell genes. Bioinformatics analysis of the IL-1 regulated gene suite revealed that inflammatory and immune response pathways are primarily elicited; likely facilitating PCa cell survival in an inflammatory tumor microenvironment. Our data supports that IL-1 reprograms AR+ PCa cells to mimic AR- PCa gene expression patterns that favor AR-targeted treatment resistance and cell survival.
2018-02-01 | GSE105088 | GEO
Project description:Activated eosinophils is a major cell type to be involved in allergic diseases. IL-5 primarily activates eosinophils and prolongs their survival. Notably, inflammatory cytokines including IL-33 and TNF-alpha are also important to establish and augment its inflammatory process in type 2 inflammation. The aim of this study is to clarify the role of these cytokines as direct activators for human eosinophils.
| PXD052708 | JPOST Repository
Project description:Activated eosinophils is a major cell type to be involved in allergic diseases. Type 2 cytokines (IL-4 and IL-5) are important to establish and augment their inflammatory process. The aim of this study is to clarify the role of these cytokines as direct activators for human eosinophils.
| PXD052200 | JPOST Repository
Project description:Memory CD8 T cells (Tmem) are activated into innate-like killers by cytokines such as IL-12, IL-15 and IL-18; but mechanisms regulating this phenomenon (termed bystander activation) are unclear. We show that basal IL-4 signals antagonize IL-18 sensing and blunt IFNg production following bystander activation of Tmem in mice. Furthermore, IL-4 treatment can act directly on Tmem in a STAT6-dependent manner, to limit their control of a bystander bacterial infection. Nevertheless, we find that IL-4 does not simply block bystander activation but rather alters Tmem gene expression to tune effector molecule expression. Defective bystander activation of homeostatic Tmem in some strains relates, in part, to IL-4 exposure, but we show that these differences are erased in Tmem produced by TCR activation leading to uniform IL-18 receptor expression and capacity for bystander activation/cytotoxicity. Our data demonstrate that bystander activation by inflammatory cytokines is subject to regulation by both IL-4 and by prior antigen experience. These findings underscore the importance of the cytokine milieu in dictating the ability of bystander CD8 Tmem to mediate pathogen control.
2026-02-01 | GSE315645 | GEO
Project description:Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. α1-ARs and β-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes. However, little is known about the functional similarities and differences between α1- and β-ARs activated temporal responses in stress-induced cardiac pathology. In this work, we systematically compared the cardiac temporal genome-wide profiles of acute α1-AR and β-AR activation in the mice model by integrating transcriptome and proteome. We found that α1- and β-AR activations induced sustained and transient inflammatory gene expression, respectively. Particularly, the overactivation of α1-AR but not β-AR led to neutrophil infiltration at 1 day, which was closely associated with the up-regulation of chemokines, activation of NF-κB pathway, and sustained inflammatory response. Furthermore, there are more metabolic disorders under α1-AR overactivation compared with β-AR overactivation. These findings provide a new therapeutic strategy that besides using β-blocker as soon as possible, blocking α1-AR within one day should also be considered in the treatment of acute stress associated cardiovascular diseases.
2023-01-19 | PXD036011 | Pride
Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.
2019-03-30 | GSE129022 | GEO
Project description:Background: Identifying the immune components that are regulated by a2NTD, a peptide cleaved from the N-terminus of the a2 vacuolar ATPase. Methods: In this study, we used pathway-focused PCR arrays to determine the genes that are regulated in human monocytic cell line, THP-1 after a2NTD stimulation over time. Results: a2NTD up-regulated several cytokines including IL-1 alpha, IL-1 beta, and IL-10. Several chemokines were also upregulated including the MCP and MIP families. Conclusion: We believe a2NTD to be an immune modulator made by tumor cells that aid in preventing immune surveillance by up-regulating proteins in monocytes that are both pro-and anti-inflammatory in nature. The Human Inflammatory Response and Autoimmunity RTM-BM-2 ProfilerM-bM-^DM-" PCR Array profiles the expression of 84 key genes involved in autoimmune and inflammatory immune responses. It represents the expression of inflammatory cytokines and chemokines as well as their receptors. It also contains genes related to the metabolism of cytokines and involved in cytokine-cytokine receptor interactions. Thoroughly researched panels of genes involved in the acute-phase response, inflammatory response, and humoral immune responses are represented as well. Using real-time PCR, you can easily and reliably analyze expression of a focused panel of genes related to inflammatory and autoimmune responses with this array.
2010-11-20 | E-GEOD-25490 | biostudies-arrayexpress
Project description:Analysis of MIN6 murine beta cell line transfected with Pla2g6 RNAi and treated with pro-inflammatory cytokines TNF-alpha, IL-1beta and IFN-gamma.
2024-02-08 | PXD017863 | Pride