Project description:In this study, we investigated the chromatin accessibility changes in human dermal fibroblasts in response to IL-1尾 stimulation, a key pro-inflammatory cytokine. Using ATAC-seq, we compared the open chromatin landscapes between control fibroblasts and those treated with IL-1尾. The data provide insights into the regulatory elements activated during fibroblast differentiation and their potential role in sustaining inflammation within the skin. These findings contribute to our understanding of fibroblast-mediated inflammation in autoimmune diseases like SLE and offer a resource for identifying novel therapeutic targets.
Project description:To gain a better understanding of the role of Interleukin-1β (IL-1β) in lung CD140a+ mesenchymal cells (fibroblasts) modulation, we performed RNA-seq to compare the transcriptomes of IL-1β-treated and control lung CD140a+ mesenchymal cells (fibroblasts).
Project description:Fibroblasts display significant heterogeneity and exhibit distinct gene expression profiles under different cytokine stimulations. We utilized RNA-seq to analyze the expression profile differences between control and IL-1β stimulated fibroblasts( n=3). Our analysis revealed 1756 differentially expressed genes between WT and Smyd1-KO hearts [adjusted P-value <0.05, |log2(fold change)| > 0.5]. Among these, 755 genes were upregulated, and 843 genes were downregulated in IL-1β stimulated human dermal fibroblasts. Notably, IL-1β stimulation can induce fibroblast differentiation into pro-inflammatory fibroblasts, characterized by the expression of neutrophil-related chemokines (CXCL1, CXCL2, CXCL3), ferroptosis-related genes (PTGS2, TNFAIP6), and pro-inflammatory cytokines (IL6). Our findings lay the groundwork for understanding the IL-1β-induced fibroblast expression of specific gene profiles.
Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients. Primary fibroblasts were obtained from HOIL-1, MYD88- and NEMO-deficient patients and healthy donors and stimulated with TNF-α or IL-1β for 2 and 6 hours. RNA were extracted and globin reduced. Labeled cRNA were hybridized to Illumina Human HT-12 Beadchips.
Project description:Neutrophils are key contributors to the pathogenesis of SLE. Using single-cell sequencing data from SLE skin lesions, we identified a subcluster of CXCL1+ fibroblasts primarily induced by IL-1β. To better understand the effects of CXCL1+ fibroblasts on neutrophils, we established a conditional culture model using culture supernatants from control and IL-1β-stimulated fibroblasts. Neutrophils were collected after 21 hours of conditional culture and subjected to RNA-seq. Our findings revealed that neutrophils exhibited a distinct pro-inflammatory phenotype, expressing higher levels of pro-inflammatory cytokines such as IL1B, TNFA, IL8, and OSM.
Project description:Analysis of response to leptin and IL-1β in gingival fibroblasts at the gene expression level. The hypothesis tested in the present study was that leptin and IL-1β synergistically effect the phenotype of gingival fibroblasts. Results provide important information regarding the response of gingival fibroblasts to leptin and IL-1β, such as specific inflammatory genes that were up- or down-regulated.
Project description:This transcriptome‑sequencing‑based study was performed to explore the transcriptional alterations triggered by stimulation with the inflammatory cytokine IL‑1β in human HCC cells. IL‑1β‑treated and vehicle‑control cell samples were harvested after 24 h of stimulation for total RNA extraction, strand‑specific library construction and high‑throughput RNA‑seq profiling. This dataset was generated to investigate the wide‑ranging biological impacts of IL‑1β‑mediated inflammatory signaling on hepatocellular carcinoma cells, and to provide transcriptomic resources for subsequent exploration of inflammation‑associated molecular events, functional pathways and candidate regulatory genes. All raw sequencing reads from this project have been deposited in the NCBI SRA database for public re‑analysis.