Expression data from human monocytes stimulated with wild-type N. meningitidis and recombinant IL-10
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PROVIDER: PRJNA324622 | ENA |
REPOSITORIES: ENA
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Project description:Background: Biological interpretation of gene expression data may differ depending on underlying assumptions and statistical tests used by the chosen bioinformatic tool. We used Gene Set Enrichment Analysis (GSEA) and Ingenuity Pathway Analysis (IPA) to analyze previously generated gene expression profiles induced in human monocytes by N. meningitidis and IL-10 (“the model system”), and by meningococcal sepsis plasma before and after immunodepletion of IL-10 (“the patient plasma system”). The objectives were to compare whether these two methods resulted in similar biological interpretation of the datasets; and identify whether GSEA provided additional insight about the human monocyte host response to meningococcal activation. Results: In both experimental models, GSEA and IPA associated genes induced in monocytes by N. meningitidis with pro-inflammatory innate immune activation, including TNF-signaling, Toll-like receptor signaling, JAK-STAT-signaling, type I and type II interferon. GSEA associated genes regulated by the presence of IL-10 with similar gene sets in both the model system and the patient plasma system. In the model system, GSEA and IPA identified 170 genes associated with oxidative phosphorylation/mitochondrial function to be down-regulated in monocytes stimulated with meningococci. In the patient plasma system, GSEA and IPA combined identified 122 genes associated with oxidative phosphorylation/mitochondrial dysfunction to be down-regulated by meningococcal sepsis plasma depleted for IL-10. Combining analyses from GSEA and IPA identified that some genes associated with oxidative phosphorylation/mitochondrial function that were inhibited by N. meningitidis were partially up-regulated by IL-10. Conclusions: Biological processes associated with the gene expression changes in the model system of meningococcal sepsis was comparable to the results found in the patient plasma system. By combining GSEA with IPA, we have discovered an inhibitory effect exerted by N. meningitidis on genes associated with oxidative phosphorylation, and that IL-10 possibly partially dampen this strong inhibitory effect, thereby identifying, to our knowledge, yet another area where IL-10 regulates the effect of LPS. We suggest that relying on a single bioinformatic tool together with arbitrarily chosen filtering criteria for data analysis may result in overlooking relevant biological processes and signaling pathways associated with genes differentially expressed between compared experimental conditions.
2016-06-08 | GSE82315 | GEO
Project description:Background: Biological interpretation of gene expression data may differ depending on underlying assumptions and statistical tests used by the chosen bioinformatic tool. We used Gene Set Enrichment Analysis (GSEA) and Ingenuity Pathway Analysis (IPA) to analyze previously generated gene expression profiles induced in human monocytes by N. meningitidis and IL-10 (“the model system”), and by meningococcal sepsis plasma before and after immunodepletion of IL-10 (“the patient plasma system”). The objectives were to compare whether these two methods resulted in similar biological interpretation of the datasets; and identify whether GSEA provided additional insight about the human monocyte host response to meningococcal activation. Results: In both experimental models, GSEA and IPA associated genes induced in monocytes by N. meningitidis with pro-inflammatory innate immune activation, including TNF-signaling, Toll-like receptor signaling, JAK-STAT-signaling, type I and type II interferon. GSEA associated genes regulated by the presence of IL-10 with similar gene sets in both the model system and the patient plasma system. In the model system, GSEA and IPA identified 170 genes associated with oxidative phosphorylation/mitochondrial function to be down-regulated in monocytes stimulated with meningococci. In the patient plasma system, GSEA and IPA combined identified 122 genes associated with oxidative phosphorylation/mitochondrial dysfunction to be down-regulated by meningococcal sepsis plasma depleted for IL-10. Combining analyses from GSEA and IPA identified that some genes associated with oxidative phosphorylation/mitochondrial function that were inhibited by N. meningitidis were partially up-regulated by IL-10. Conclusions: Biological processes associated with the gene expression changes in the model system of meningococcal sepsis was comparable to the results found in the patient plasma system. By combining GSEA with IPA, we have discovered an inhibitory effect exerted by N. meningitidis on genes associated with oxidative phosphorylation, and that IL-10 possibly partially dampen this strong inhibitory effect, thereby identifying, to our knowledge, yet another area where IL-10 regulates the effect of LPS. We suggest that relying on a single bioinformatic tool together with arbitrarily chosen filtering criteria for data analysis may result in overlooking relevant biological processes and signaling pathways associated with genes differentially expressed between compared experimental conditions.
2016-06-08 | GSE82166 | GEO
Project description:Meningococcal sepsis is an overwhelming form of the sepsis syndrome which may cause mortality within 12-24 hours in previously healthy children and adults, where the causative infectious agent is N. meningitidis, an obligate human pathogen. The genomic changes induced by N. meningitidis are modulated by the anti-inflammatory cytokine interleukin-10 (IL-10), which is present in large quantities in plasma from patients with meningococcal sepsis. This present study investigated kinase activities in human monocytes stimulated by N. meningitidis and IL-10. The first aim was to identify array peptides that could indicate which signaling pathways were activated or inhibited by the host response to the meningococci. The second aim was to detect whether IL-10 affected N. meningitidis-nduced phosphorylation of array peptides, in order to identify potential targets of the IL-10 anti-inflammatory response. We approached this using a strategy where elutriation-purified human monocytes are stimulated in vitro with N. meningitidis and IL-10, with concentrations corresponding to previously measured levels in patients with fulminant meningococcal septicemia. This work examined activation or inhibition of signaling pathways mediated by tyrosine kinases when purified human monocytes are in vitro incubated with N. meningitidis in the presence or absence of IL-10.
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2016-06-08 | GSE82316 | GEO
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2021-03-04 | PXD024515 |
Project description:CD14+ Monocytes from healthy volunteers were purified by MACS (negative selection) and FACSorting and either left untreated or stimulated for 24h and 48h with LPS. THP-1 cells were stimulated for 4h, 24h and 48h with LPS. Glycoproteins were captured with hydrazide chemistry and tryptic and PNGase F-released peptide fractions analyzed by MS/MS. Quantitative assessment revealed differential glycoprotein expression in activated/LPS-tolerized monocytes and naïve monocytes and THP-1 cells.
2017-04-24 | PXD004034 | Pride
Project description:CD14+ monocytes were separated from human peripheral blood and exposed to IL-4 for 12 or 72 hours then subjected to microarray analysis We used Affymetrix miRNA1.0 microarray to obtain global miRNA expression data of human monocytes, unstimulated and IL-4-stimulated differentiating macrophages.
2016-04-29 | GSE71641 | GEO
Project description:Background: Monocytes play a crucial role in innate immune responses for host defense, yet their involvement in chronic obstructive pulmonary disease (COPD) remains poorly understood. We previously identified a subset of monocytes in COPD lung tissues characterized by high interleukin-6 receptor (IL-6R) expression. This study aimed to characterize the phenotypes of IL-6Rhi monocytes in the lung of COPD patients. Methods: Using flow cytometry, we assessed the abundance of pulmonary CD14+IL-6Rhi cells in never smokers (CNS), control ex-smokers (CES) and COPD patients. IL-6 expression in CD14+ monocytes from peripheral blood of patients with COPD was also examined. CD45+CD206–CD14+IL-6Rhi and CD45+CD206–CD14+IL-6R– cells were isolated from COPD lung tissues for transcriptome analysis. A monocyte line THP1 cell with constitutive IL-6R expression was stimulated with recombinant IL-6, followed by RNA sequencing to evaluate IL-6 responsiveness of IL-6R+ monocytes. Results: The number of pulmonary CD14+IL-6Rhi monocytes was elevated in COPD patients compared to CNS, while CD14+ monocytes in the peripheral blood of COPD patients did not express IL-6R. Upregulated mRNA expression in CD14+IL-6Rhi monocytes was associated with chemotaxis, monocyte differentiation, fatty acid metabolism and integrin-mediated signaling pathway. Stimulation of THP1 cells with recombinant IL-6 induced gene expression changes linked to chemotaxis and organism development. Conclusion: In patients with COPD, CD14+IL-6Rhi monocytes increase in lung tissues compared to CNS and exhibit a different transcriptome profile from CD14+IL-6R– monocytes.
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