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:Analysis of the effects of AVS023 and its active compounds (gallic acid and piperine) on human gene expression in primary human dermal fibroblasts induced by IL-1β. The results provided up- and down- regulated genes resulting from IL-1β and IL-1β plus with each test compound in primary human dermal fibroblasts
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: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: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: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:This study shows that, in the presence of CD4+ T cells, dermal fibroblasts shift towards an antimicrobial phenotype leading to reduced dermal invasion by C. albicans. This is dependent on TLR2 activation and pro-IL-1β cleavage and results in expression of genes involved in defense against various classes of pathogens.
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.