RNA-seq of IL-13 activated human schwann cell compared with control human schwann cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE218436 | GEO | 2023/06/14
REPOSITORIES: GEO
Similar Datasets
Project description:RNA-seq of IL-13 activated human schwann cell compared with control human schwann cell
| PRJNA903840 | ENA
Project description:It has been previously shown that airway exposure to Toll-like receptor ligands through lipopolysaccharide (LPS)-contaminated house dust or bacterial infections can exacerbate allergic inflammation; however, the underlying mechanism(s) controlling this response have not been fully elucidated. Here we report that basophils are the major source of Th2 cytokines that respond to TLR4 ligands, such as LPS and lipid A, in human PBMC and murine spleen cells. LPS activated human PBMCs to up-regulate mRNAs for not only pro-inflammatory cytokines such as IL-6 and chemokines such as CXCL8 (IL-8), CCL2 (MCP-1), but also Th2 cytokines such as IL-4 and IL13. Among PBMCs, we identified CD123+/BDCA4- basophils as the major source of IL-4 and IL-13 in response to LPS. Even in the absence of IgE, purified human basophils, as well as a basophilic cell line, were directly activated by LPS to produce IL-4 and IL-13. Moreover, LPS-stimulated IL-4 knockin mouse (4get mice) spleens identified the basophils as the major IL-4 producing cells in a TLR4-dependent manner. These results indicate that bacterial LPS may play a role in type-2 immunity through direct activation of basophils to produce IL-4 and IL-13. Keywords: Cell type comparison
2013-12-31 | GSE8589 | GEO
Project description:Schwann cells (SCs) proliferation is crucial for axonal guidance and nerve regeneration following nerve injury. This study aims to investigate the in vitro effects of interleukin-22 (IL-22) on SCs and the corresponding mechanism.
2018-06-15 | GSE69866 | GEO
Project description:Osteoarthritis is a chronic disease characterised by the loss of articular cartilage in synovial joints through a process of extracellular matrix destruction that is strongly associated with inflammatory stimuli. Chondrocytes undergo changes to their protein translation capacity during osteoarthritis, but a study of how disease-relevant signals effect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study we describe how the inflammatory cytokine interleukin 1-beta (IL-1β) rapidly affects protein translation in the chondrocytic cell line SW1353. Using ribosome profiling we demonstrate that IL-1β induced altered translation of inflammatory-associated transcripts such as NFKB1, TNFAIP2, MMP13, CCL2 and CCL7, as well as a number of ribosome-associated transcripts, through differential translation and the use of multiple open reading frames. Proteomic analysis of the cellular layer and the conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. These translationally regulated secreted proteins included a number of chemokines and cytokines, underlining the rapid, translationally-mediated inflammatory cascade that is initiated by IL-1 β.
2019-07-12 | E-MTAB-7466 | biostudies-arrayexpress
Project description:Fibroblasts are primary structural cells involved in tissue remodelling, but recent transcriptomic data have highlighted the ability of fibroblasts to display molecules that contribute to inflammation. Which factors might drive such inflammatory phenotypes are unclear. LIGHT (TNFSF14) is a cytokine that we previously showed was involved in inflammation of the lungs and may be central to lung diseases exhibiting fibrosis and inflammation, including asthma and interstitial lung disease. With RNA-seq, we investigated the activity of LIGHT in human pulmonary fibroblasts compared to IL-13 and IL-17, two other cytokines linked to lung disease. While all three cytokines individually induced both unique and overlapping gene transcripts, when fibroblasts were stimulated with LIGHT and IL-13 they upregulated more inflammatory transcripts including CCL2, CCL26, CXCL2, CXCL3, CXCL5, CXCL6, IL32, CSF2, VCAM1, ICAM1, IL18R1, IL1RL1, TNFRSF12A, TNFRSF4, TNFRSF8, ITGA2, ITGA4, and ITGAV; and when stimulated with LIGHT and IL-17, inflammatory transcripts included CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL8, IL32, IL33, CSF2, TSLP, IL1A, IL6, IL18, VCAM1, ICAM1, IL18R1, IL1RL1, TNFSF4, TNFRSF4, TNFRSF8, ITGA2, ITGA4, and ITGAV. Furthermore, multiple cell cycle-related transcripts were induced with the combinations of LIGHT with IL-13 or IL-17. Providing physiological significance, some of the fibroblast transcriptional signatures induced by these cytokines were found to be present in subsets of fibroblasts isolated from patients with interstitial lung disease. This study highlights the synergistic activities of LIGHT in lung fibroblasts and suggests it could drive inflammatory activities relevant for several diseases dependent on the availability of other classical cytokines made in the lungs.
2025-07-10 | GSE295622 | GEO
Project description:A protocol was established for the derivation of Schwann cell-like cells from human BMSCs. The commitment to the Schwann cell fate was acquired by Schwann cell-like cells in co-culture with rat DRG neurons. Microarray analysis provided evidence that the human BMSC-derived Schwann cells were functionally mature.
2017-08-01 | GSE102049 | GEO
Project description:Allergic asthma is a chronic inflammatory airway disease driven by the cytokine interleukin-13 (IL-13). Although IL-13 signals through the canonical JAK1/TYK2/STAT6 pathway, our understanding of the totality of IL-13-induced signaling intermediates is incomplete. To address this, we performed an unbiased phospho-proteomic analysis of IL-13-stimulated A549 human airway epithelial cells. IL-13 stimulation led to differential phosphorylation at 145 unique serine/threonine residues across 97 proteins involved in diverse cellular processes. These processes included RNA splicing, cytoskeletal remodeling, GTPase activity, and focal adhesion complex formation. Network analysis identified SRC, a non-receptor tyrosine kinase, as a potential upstream regulator of IL-13-induced changes in phosphorylation. Kinetic molecular approaches confirmed that SRC is rapidly activated following IL-13 stimulation, prior to activation of the canonical IL-13 signaling intermediate STAT6 in both human and mouse lung fibroblasts. Pharmacological inhibition of SRC reduced IL-13–induced STAT6 phosphorylation and downstream gene expression in vitro. In vivo, SRC antagonism attenuated IL-13–induced airway hyperresponsiveness (AHR) without significantly affecting inflammatory cell infiltration or gene expression in bronchoalveolar lavage fluid. These findings identify SRC as a novel and selective mediator of IL-13–driven airway responses and suggest that targeting SRC may offer therapeutic benefit in allergic asthma.
2025-12-05 | PXD066489 | Pride
Project description:Schwann cell maturation is tightly controlled by a set of transcriptional regulators. We have deleted the zinc-finger transcription factor Sip1 specifically from immature Schwann cells and observed a dramatic developmental delay. In an attempt to define the developmental stage of Sip1-deficient Schwann cells, we performed microarray analysis of Schwann cell-specific mutants compared to controls at the age of 25 days (P25).
2016-06-13 | GSE76027 | GEO
Project description:Human neutrophils stimulated with IL-13.
| PRJNA558811 | ENA
Project description:Schwann cell maturation is tightly controlled by a set of transcriptional regulators. We have deleted the zinc-finger transcription factor Sip1 specifically from immature Schwann cells and observed a dramatic developmental delay. In an attempt to define the developmental stage of Sip1-deficient Schwann cells, we performed microarray analysis of Schwann cell-specific mutants compared to controls at the age of 25 days (P25). Sciatic nerves of 3 mutant mice and 3 corresponding controls were isolated at the age of 25 days.
2016-06-13 | E-GEOD-76027 | biostudies-arrayexpress