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IL-36R stimulation of colonic mouse fibroblasts

ABSTRACT: IL-36R stimulation of colonic mouse fibroblasts

PROVIDER: PRJEB10270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR979804.fastq.gz	Fastqsanger.gz
	ERR979805.fastq.gz	Fastqsanger.gz
	ERR979806.fastq.gz	Fastqsanger.gz
	ERR979807.fastq.gz	Fastqsanger.gz
	ERR979808.fastq.gz	Fastqsanger.gz

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IL-36R stimulation of colonic mouse fibroblasts

Project description:Intestinal fibroblasts from the colons of C57BL/6 wild-type mice were grown in the presence or absence of IL-36ÉŁ (30 ng/ml) for 4 hours. The experimental setup included 6 samples from 3 colons in a pairwise design (3 stimulated vs 3 unstimulated). Profiling of whole-genome transcriptomic patterns was performed with 1.2 Âľg high quality total RNA per sample by RNA-seq at the Next Generation Sequencing core unit of the university hospital Erlangen. The sequencing platform was Illumina HiSeq-2500 with high output mode and single-end 100bp fragments. The sequencing library was NuGEN Ovation RNA-Seq Library Prep-Kit. Demultiplexed reads were corrected regarding rRNAs, tRNAs, mt-rRNAs and mt-tRNAs. Alignment against the mus musculus reference genome (Ensemble version 75 for GRCm38) was performed with RNAseq aligner STAR (version 2.4.0.i) and quantification (HTseq count) was done of unique mappings.

2015-12-31 | E-MTAB-3814 | biostudies-arrayexpress

Transcriptional profiling of long-term stimulated primary murine intestinal fibroblasts with interleukin-36.

Project description:Previous stimulation experiments of stimulated primary murine colonic fibroblasts with IL-36R ligands for 4h in vitro showed an upregulation of pro-inflammatory cytokines e.g. IL-6, IL-1b and chemokines e.g. CXCL1, CCL2 indicating an important role for IL-36 in inflammation. We were interested in analyzing long-term stimulation (9 days) of intestinal fibroblasts to identify a putative differential expression profile. The experimental setup included 6 samples from 3 colons in a pairwise design (3 stimulated vs 3 unstimulated).

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Enhanced IL-36R signaling promotes barrier impairment and inflammation in skin and intestine

Project description:Deficiency in IL-36R antagonist caused by loss of function mutations in IL-36RN leads to DITRA (1), a rare inflammatory human disease that belongs to a subgroup of Generalized Pustular Psoriasis (GPP). Herein, we report a novel functional genetic mouse model of DITRA with enhanced IL-36R signaling analogous to one observed in DITRA patients which supports and provides new insight in our understanding of IL-36 family of molecules in regulating barrier integrity across multiple tissues. Humanized DITRA-like mice displayed increased skin inflammation in preclinical model of psoriasis, and in vivo blockade of IL-36R pathway using anti-human IL-36R antibody ameliorated IMQ-induced skin pathology at both prophylactic and therapeutic treatments. Deeper characterization of the humanized DITRA-like mice revealed that deregulated IL-36R signaling promoted tissue pathology during intestinal injury and led to impairment in mucosal restoration in the repair phase of chronic DSS-induced colitis. Blockade of IL-36R pathway significantly ameliorated DSS-induced intestinal inflammation and rescued the inability of DITRA-like mice to recover from mucosal damage in vivo. Thus, our results indicate a central role for IL-36 in regulating the pro-inflammatory responses in the skin and epithelial barrier function in the intestine suggesting a new therapeutic potential for IL-36R axis in psoriasis and at the later stages of intestinal pathology.

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Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. The supernatants from the co-culture of UV-aged mouse primary keratinocytes with synovial fibroblasts were collected to induce mouse primary articular chondrocytes (CCs) to become aging SNL CCs. On this basis, Spesolimab (100ng/ml) was added to culture aging SNL CCs to study the drug's effect on OA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 3 groups: control CCs, aging SNL CCs, aging SNL CCs+Spesolimab.

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Aged skin exacerbates experimental osteoarthritis via enhanced IL-36R signaling

Project description:To investigate skin aging is an important driver of experimental osteoarthritis(OA) progression in mice via enhanced IL-36 receptor (IL-36R) signaling. we generated epidermis keratinocyte conditional knockout mice (IL-36Ra-cKO) with topical administration of capsid-mutant Adeno-associated virus 2 (AAV2) vector23 encoding Cre recombinase (AAV2-Cre) to IL-36Rafl/fl mice. Subsequently, epidermal skin tissues were collected from IL-36Rafl/fl and IL-36Ra-cKO mice for RNA sequencing analysis.

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Project description:The DEAD-box (DDX) proteins function in diverse cellular processes including RNA alternative splicing, and are linked to immune-mediated diseases. However, little is known about the roles of DDXs in skin inflammatory diseases. Here, we show that DDX5, one of the founding members of the DDX RNA helicase family, controls skin inflammation and participates in the pathogenesis of psoriasis via regulating IL-36R pre-mRNA splicing. We found that both mRNA and protein of DDX5 are decreased in lesional skin from patients with psoriasis and psoriasis-like mice, and that mice with keratinocyte-specific ablation of DDX5 spontaneously develop psoriasis-like phenotypes. Mechanistically, DDX5 complexes with serine/arginine-rich splicing factor 1(SRSF1) to typically regulate IL-36R pre-mRNA splicing in keratinocytes, which generates mRNAs encoding full-length IL-36R and a previously unknown soluble form of IL-36R (sIL-36R). sIL-36R controls IL-36/IL-36R signaling by competing with IL-36R for IL-36γ ligation. The reduction or deficiency of DDX5 leads to IL-36R pre-mRNA splicing preferring to the generation of IL-36R but not sIL-36R, thereby selectively amplifying inflammatory responses of keratinocytes to IL-36γ and then aggravating cutaneous inflammation in psoriasis. Genetic restoration or intradermal administration of sIL-36R in psoriasis-like mice suppresses IL-36R signaling and alleviates the disease phenotype of psoriasis. Altogether, these data reveal a pathogenic role of DDX5 during psoriasis, and provide mechanistic insights into the regulation of IL-36R splicing and its impact on psoriasis development.

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