Transcriptomics of THP-1 macrophages treated with or without IL-26 for 24h
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ABSTRACT:
PROVIDER: PRJNA791656 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17311829_1.fastq.gz | Fastqsanger.gz | |||
| SRR17311829_2.fastq.gz | Fastqsanger.gz | |||
| SRR17311830_1.fastq.gz | Fastqsanger.gz | |||
| SRR17311830_2.fastq.gz | Fastqsanger.gz | |||
| SRR17311831_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The aim of this study was to obtain a comprehensive transcriptomic analysis of IL-26-exposed macrophages. Methods: THP-1 derived macrophage were generated by incubating THP-1 cells with PMA (50 ng/ml) for 24h.Then THP-1 macrophages were treated with IL-26 for 24h, which were collected and applied to RNA-sequencing. The constructed sequencing library was sequenced using an Illumina Novaseq 6000 system. The expression of transcripts was calculated as fragments per kilobase of exon model per million mapped reads (FPKM). Results: In total, we identified 1303 differentially expressed protein-coding genes between untreated and IL-26-treated macrophages, including 667 up-regulated and 636 down-regulated genes.
2022-04-27 | GSE192493 | GEO
Project description:Purpose: To investigate the inhibition of inflammatoty cytokines of Hydroxychloroquine to phagocytic THP-1 cells. Methods: we established a cell model of hemophagocytosis by simulating THP-1 cells with CpG-c for 24h in vitro to produce macrophages, and then coculture the cells with human RBCs. RNA sequencing analysis of THP-1 cells were performed to find Gene changed with CpG-c stimulation and Hydroxychloroquine intervention. Results:CpG-c sitimulation significantly altered gene expression of THP-1 cells. Cytokine genes were upregulated, especially a significant increase in IL-6 level from scratch. HCQ significantly inhibited the expression of inflammatory cytokines and decreased IL-6 gene level to baseline. Conclusions:Hydroxychloroquine can inhibite cytokine genes, especially IL-6 Gene level of THP-1 cells caused by CpG-c sitimulation.
2022-07-01 | GSE198290 | GEO
Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
2025-07-01 | GSE300682 | GEO
Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
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Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
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Project description:Animals host symbiotic microbial communities that shape gut health. However, how the host immune system and microbiota interact to regulate epithelial homeostasis, particularly during early development, remains unclear. Human interleukin-26 (IL-26) is associated with gut inflammation and has intrinsic bactericidal activity in vitro, yet its in vivo functions are largely unknown, primarily due to its absence in rodents. To examine the role of IL-26 in early life, we used zebrafish and found that gut epithelial cells in il26-/- larvae exhibited increased proliferation, faster turnover, elevated and DNA damage response, and altered cell population abundance. This epithelial dysregulation occurred independently of the IL-26 canonical receptor and resulted from dysbiosis in il26-/-. Moreover, IL-26 bactericidal activity was conserved in zebrafish, suggesting a potential role of this property in regulating microbiota composition. We further identified innate lymphoid cells (ILCs) as the primary source of IL-26 at this developmental stage. These findings establish IL-26 as a central player in a regulatory circuit linking the microbiota, ILCs, and intestinal epithelial cells to maintain gut homeostasis during early life.
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Project description:THP-1 cells were treated with phorbol 12-myristate 13-acetate (PMA) at 25μg/ml for 48h.Then remove PMA and rest for 24h to obtain M0 macropahges. Further applied LPS and IFNγ or IL-4 and IL-13 for 24h to obtain M1, M2 macrophages, respectively. During polarization, cells were growth within control medium(LN) or medium with extra lipid mixture(LH).M0,M1,M2 cells were collected and applied to RNA-sequencing. We found that differential activation of macrophage had distinct metabolic signature.Extra lipids supplement did not significantly alter transcriptomes of macrophages.
2021-06-28 | GSE159112 | GEO
Project description:THP-1 cells were treated with phorbol 12-myristate 13-acetate (PMA) at 25μg/ml for 48h.Then remove PMA and rest for 24h to obtain M0 macropahges. Further applied LPS and IFNγ or IL-4 and IL-13 for 24h to obtain M1, M2 macrophages, respectively. During polarization, cells were treated with prostaglandin E2 or MEHP.Then M1,M2 cells were collected and applied to RNA-sequencing. We found that PGE2 and MEHP significantly impacted metabolic signature of macrophages.
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