Next Generation Sequencing reveals different transcriptome induced by IL4-10 fusion protein (IL4-10 FP) compared to the combination of cytokines in mice with inflammatory pain
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ABSTRACT:
PROVIDER: PRJNA633598 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11808625.fastq.gz | Fastqsanger.gz | |||
| SRR11808626.fastq.gz | Fastqsanger.gz | |||
| SRR11808627.fastq.gz | Fastqsanger.gz | |||
| SRR11808628.fastq.gz | Fastqsanger.gz | |||
| SRR11808629.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: The goalsof this study was to compare the transcriptome profiling of dorsal root ganglia (DRG) of animals injected intrathecally with IL4-10 FP, the combination of IL4+IL10 or vehicle, one week after induction of persistent inflammatory pain. Methods: Mice received an intraplantar injection of carrageenan and one week developing inflammatory pain were intrathecally injected with IL4-10 FP, IL4+IL10 or PBS. DRGs were isolated and RNA libraries were prepared with the poly A selection method followed by multiplexing and sequencing on the Illumina NextSeq500® platform in a 1 × 75bp single-read and 350 million reads per lane (Utrecht Sequencing Facility) Results: In vivo IL4-10 FP induces a differential transcriptome than the combination of cytokines in mice with persistent inflammatory pain. Conclusions: The superior analgesic effect observed in mice treated with IL4-10 FP compared to mice injected with the naïve cytokines is derived from an induction of a different transcriptome on the lumbar DRGs.
2021-02-28 | GSE150795 | GEO
Project description:We purposed to examine the effect of PGF receptor FP in development of ; bleomycin-induced pulmonary fibrosis in mice. We performed gene ; expression analysis in the lung of WT and FP-KO mice on Days 0, 7 and ; 14. We found out that fibrosis-related genes such as various isoforms ; of collagen, which were induced on Day 7 and continued to increase or ; remained unchanged on Day 14, were induced to less extent in FP-KO ; mice. In contrast, expression of inflammation-related genes peaked on ; Day 7 similarly in WT and FP-KO mice. These results suggest that FP ; functions in fibrosis-phase, not in peak inflammation phase, and ; facilitates fibrogenesis by enhancing expression of fibrosis-related ; genes. Experiment Overall Design: RNA was prepared from the lung of WT and FP-KO mice on Day 0, 7 and 14 Experiment Overall Design: (n=4-5 for each group at each time point) after bleomycin instillation, Experiment Overall Design: and used for hybridization with Affymetrics mouse 430 2.0 microarrays. Experiment Overall Design: Time-dependent changes in expression of genes in FP-KO mice were Experiment Overall Design: compared with those in WT mice.
2009-11-11 | E-GEOD-18800 | biostudies-arrayexpress
Project description:We purposed to examine the effect of PGF receptor FP in development of bleomycin-induced pulmonary fibrosis in mice. We performed gene expression analysis in the lung of WT and FP-KO mice on Days 0, 7 and 14. We found out that fibrosis-related genes such as various isoforms of collagen, which were induced on Day 7 and continued to increase or remained unchanged on Day 14, were induced to less extent in FP-KO mice. In contrast, expression of inflammation-related genes peaked on Day 7 similarly in WT and FP-KO mice. These results suggest that FP functions in fibrosis-phase, not in peak inflammation phase, and facilitates fibrogenesis by enhancing expression of fibrosis-related genes.
2009-10-30 | GSE18800 | GEO
Project description:Purpose: Using RNA-sequencing, determine the effect of corticosteroids on human airway smooth muscle cells (ASM) exposed to Th1 and/or Th17 cytokines. Effects of cytokines and/or corticosteroids on gene expression was assessed. Methods: Pediatric human ASM (ages 0-21; n=4/treatment group) were serum starved for 48 h and then treated with 10 ng/mL TNFα, IFNγ, IL-17A, TNFα/IFNγ, or IFNγ/IL-17A in the presence of vehicle (0.01% DMSO) or 10 nM fluticasone propionate (FP). Cells were harvested after 18 h for RNA isolation, QC, library prep, and RNA sequencing on the Illumina HiSeq4000 platform. RNA quality and integrity was determined by gel electrophoresis and Agilent 2100 Bioanalyzer. Following sequencing. FASTQ files were processed and analyzed to generate counts files and perform differential expression analysis. Results: Our analyses show that cytokines, particularly TNFα, IFNγ, and TNFα/IFNγ had significant effects on gene expression. Differentially expressed genes were largely related to pro-inflammatory responses. Interestingly, we found that IL-17A had only modest effects on gene expression. Corticosteroids (FP) reduced or inhibited the effects of pro-inflammatory cytokines. However, these anti-inflammatory effects were reduced in cells treated with TNFα/IFNγ or IL-17A/IFNγ. Conclusions: These studies highlight the differential effects of pro-inflammatory cytokines and corticosteroids on gene expression in human ASM.
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Project description:Cytokines are key regulators of tumor immune surveillance by controlling immune cell activity. Here, we investigated whether interleukin 4 (IL4) has antileukemic activity via immune-mediated mechanisms in an in vivo murine model of acute myeloid leukemia driven by the MLL-AF9 fusion gene. Although IL4 strongly inhibited leukemia development in immunocompetent mice, the effect was diminished in immune-deficient recipient mice, demonstrating that the antileukemic effect of IL4 in vivo is dependent on the host immune system. Using flow cytometric analysis and immunohistochemistry, we revealed that the antileukemic effect of IL4 coincided with an expansion of F4/80+ macrophages in the bone marrow and spleen. To elucidate whether this macrophage expansion was responsible of the antileukemic effect, we depleted macrophages in vivo with clodronate liposomes. Macrophage depletion eliminated the antileukemic effect of IL4, showing that macrophages mediated the IL4-induced killing of leukemia cells. In addition, IL4 enhanced murine macrophage-mediated phagocytosis of leukemia cells in vitro. Global transcriptomic analysis of macrophages revealed an enrichment of signatures associated with alternatively activated macrophages and increased phagocytosis upon IL4 stimulation. Notably, IL4 concurrently induced Stat6-dependent upregulation of CD47 on leukemia cells, which suppressed macrophage activity. Consistent with this finding, combining CD47 blockade with IL4 stimulation enhanced macrophage-mediated phagocytosis of leukemia cells. Thus, IL4 has two counteracting roles in regulating phagocytosis in mice; enhancing macrophage-mediated killing of leukemia cells, but also inducing CD47 expression that protects target cells from excessive phagocytosis. Taken together, our data suggests that combined strategies that activate macrophages and block CD47 have therapeutic potential in AML.
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Project description:Inflammation plays a role in neuropathic pain conditions as well as in pain induced solely by an inflammatory stimulus. Robust mechanical hyperalgesia and allodynia can be induced by locally inflaming the L5 dorsal root ganglion (DRG) in rat. This model allows investigation of the contribution of inflammation per se to chronic pain conditions. Most previous microarray studies of DRG gene expression have investigated neuropathic pain models involving axon transection. To examine the role of inflammation, we used microarray methods to examine gene expression 3 days after local inflammation of the L5 DRG in rat. We observed significant regulation in a large number of genes (23% of observed transcripts), and examined 221 (3%) with a fold-change of 1.5-fold or more in more detail. Immune-related genes were the largest category in this group and included members of the complement system as well as several pro-inflammatory cytokines. However, these upregulated cytokines had no prior links to peripheral pain in the literature other than through microarray studies, though most had previously described roles in CNS (especially neuroinflammatory conditions) as well as in immune responses. The L5 dorsal root ganglion (DRG) was locally inflamed with zymosan/Incomplete Freund's Adjuvant. DRG were isolated 3 days later. Each sample was RNA extracted from a single DRG. 6 samples from rats with local DRG inflammation were compared with 6 samples from sham-operated rats.
2012-06-21 | E-GEOD-38859 | biostudies-arrayexpress
Project description:Multiple lines of evidence indicate that immune signaling can impact the pathological progression in Alzheimer’s disease (AD), including amyloid deposition, tau aggregation, synaptic pathology and neurodegenerative trajectory. In earlier studies, we reported that intracerebral expression of the anti-inflammatory cytokines, Interleukin-10 (Il10) and Interleukin-4 (Il4), increased amyloid β (Aβ) burden in TgCRND8 mice, a preclinical model of AD-type amyloidosis. As both Interleukin-10 receptor (IL10R) and Interleukin-4 receptor (IL4R) are upregulated in an age-progressive manner in rodent models of AD and in specific regions of human AD brains, we hypothesized that a decoy receptor strategy specifically targeting Il10 and Il4 signaling could have a disease-modifying effect. We derivatized the ectodomains of mouse Il10R (sIl10R) and mouse Il4R (sIl4R) into corresponding recombinant solubilized receptor forms and delivered these intracranially into neonatal TgCRND8 mice or hippocampally into adult TgCRND8 mice with pre-existing Aβ deposits. AAV-mediated expression of sIl10R and sIl4R robustly attenuated Aβ burden in TgCRND8 mice when expressed neonatally while in the hippocampus injection cohort, AAV-sIl4R, but not sIl10R, reduced Aβ burden. sIl10R and sIl4R had opposing effects on microglial and astrocyte proliferation, with sIl10R generally reducing gliosis. RNAseq analysis showed that sIl10R likely acts as a microglial immune checkpoint inhibitor while both sIl10R and sIl4R expression show unexpected impacts on genes related to circadian rhythm. Notably, neither Il10 nor sIl10R expression altered tau pathology in two tau transgenic models, despite robust expression and impacts on glial proliferation. Together, these data reveal that decoy receptor mediated targeting of physiological Il10 or Il4 signaling can beneficially impact amyloid deposition and thus represent novel immunomodulatory approaches for AD therapy.
2025-10-01 | GSE309404 | GEO
Project description:In order to fully characterize emodin's effects on macrophage alternative activation, peritoneal macrophages were stimulated with IL4 with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IL4 induced changes in a large percentage of genes (60%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M2 macrophage activation including: Arg1, Chi3l3, and CD206. Three-condition, one-color experiment: Vehicle control, IL4 or IL4-Emodin treated periferal WBC PMN samples: 4 biological replicates each.
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