RNA-Seq analysis of IL-23 induced skin transcriptome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA552686 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9644300.fastq.gz | Fastqsanger.gz | |||
| SRR9644301.fastq.gz | Fastqsanger.gz | |||
| SRR9644302.fastq.gz | Fastqsanger.gz | |||
| SRR9644303.fastq.gz | Fastqsanger.gz | |||
| SRR9644304.fastq.gz | Fastqsanger.gz |
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Project description:Psoriasis is a complex inflammatory disease resulting from the activation of T helper (Th) 1 and Th17 cells. Recent evidence suggests that abnormal activation of Toll-like receptors (TLRs) 7, 8 and 9 contributes to the initiation and maintenance of psoriasis. We have evaluated the effects of TLR antagonists on the gene expression profile in an IL-23-induced skin inflammation model in mice. Psoriasis-like skin lesions were induced in C57BL/6 mice by intradermal injection of IL-23 in the dorsum. Two TLR antagonists were compared: IMO-3100, an antagonist of TLRs 7 and 9, and IMO-8400, an antagonist of TLRs 7, 8 and 9, both of which previously have been shown to reduce epidermal hyperplasia in this model. Skin gene expression profiles of IL-23-induced inflammation were compared with or without TLR antagonist treatment. IL-23 injection resulted in alteration of 5100 gene probes (fold change ≥ 2, FDR < 0.05) including IL-17 pathways that are up-regulated in psoriasis vulgaris. Targeting TLRs 7, 8 and 9 with IMO-8400 resulted in modulation of more than 2300 mRNAs while targeting TLRs 7 and 9 with IMO-3100 resulted in modulation of more than 1900 mRNAs. Both agents strongly decreased IL-17A expression (>12-fold reduction), normalized IL-17 induced genes such as beta-defensin and CXCL1, and normalized aberrant expression of keratin 16 (indicating epidermal hyperplasia). These results suggest that IL-23-driven inflammation in mouse skin may be dependent on signaling mediated by TLRs 7, 8, and 9 and that these receptors represent novel therapeutic targets in psoriasis vulgaris and other diseases with similar pathophysiology. Expression profiles for mice with IL23-induced phenotype (psoriasisform) at baseline and after treatment with two doses of TLR7/8/9 antagonist and saline. Samples for nomal mice are also available
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2014-01-21 | GSE50400 | GEO
Project description:IL-36R signaling plays an important role in the pathogenesis of psoriasis. We ought to assess the specific function of IL-36R in keratinocytes for the pathology of Aldara®-induced psoriasis-like skin inflammation. Il36r-/- (KO) and Il36rΔK (DK) mice as well as their littermate controls, respectively Il36r+/+ (WT) and Il36rfl/fl (FL) mice, were challenged with the topical application of Aldara® on one ear during 3 or 7 days. RNASeq was performed on treated (AL) and untreated (CT) ears. Fold change analysis combined with RPKM and RT-qPCR allowed us to identify genes which were specifically regulated by IL-36R signaling in keratinocytes during the course of the treatment. We notably demonstrated that both IL-23 subunits (Il23a and Il12b) fell into this category.
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Project description:Background & Aims: The IL-23/IL-17 axis plays an important role in the pathogenesis of autoimmune diseases and the pathological consequences of infection. We previously showed that immunopathologic mechanisms mediated by inflammatory monocytes underlie the severe focal liver damage induced by the protozoan parasite, Entamoeba histolytica. Here, we analyze the contribution of the IL-23/IL-17 axis to the induction and subsequent recovery from parasite-induced liver damage. Methods: IL-23p19-/-, IL-17A/F-/-, CCR2-/-, and WT mice were intra-hepatically infected with E. histolytica trophozoites and disease onset and recovery were analyzed by magnetic resonance imaging. The expression of liver-specific genes and proteins during infection was examined by qPCR, microarray, FACS analysis and immunohistochemistry. Immuno-depletion and substitution experiments were performed in IL-23p19-/- and WT mice to investigate the role of IL-13 in disease outcome. Results: Liver damage in infected IL-23p19-/-, IL-17A/F-/-, CCR2-/- mice was strongly attenuated compared with that in WT mice. IL-23p19-/- mice showed reduced expression of IL-17 and CCL2 genes and proteins. Increased numbers of IL-13-producing CD11b+Ly6Clo regenerative monocytes were associated with disease attenuation in IL-23p19-/- mice. Immuno-depletion of IL-13 in IL-23-/- mice reversed this attenuation and treatment of infected WT mice with an IL-13/anti-IL-13-mAb complex supported liver recovery. Conclusions: The IL-23/IL-17 axis plays a critical role in the immunopathology of hepatic amebiasis. IL- 13 secreted by CD11b+Ly6Clo monocytes supports recovery from liver damage. An IL-13/anti-IL13- mAb complex mimics this function, suggesting a novel therapeutic option to support tissue healing after liver damage.
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