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: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: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: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: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:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils. Lesional skin biopsies obtained from C57BL/6J WT mice or IL-1R-deficient mice at 4 hours post-infection with Staphylococcus aureus. Uninfected skin biopsies were also collected from WT and IL-1R-deficient mice.
Project description:To investigate the effects of IL-1β/IL-6/PGE2 on neutrophil modulation, we performed RNA-seq to compare IL-1β/IL-6/PGE2-treated neutrophils to vehicle-treated neutrophils.