Pilot study of transcriptomic responses to IL13 and HRV-A and their interaction
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA667927 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12789629_1.fastq.gz | Fastqsanger.gz | |||
| SRR12789629_2.fastq.gz | Fastqsanger.gz | |||
| SRR12789630_1.fastq.gz | Fastqsanger.gz | |||
| SRR12789630_2.fastq.gz | Fastqsanger.gz | |||
| SRR12789631_1.fastq.gz | Fastqsanger.gz |
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2011-06-30 | GSE24403 | GEO
Project description:Scleroderma is a lethal and currently irreversible autoimmune disease characterized by widespread tissue fibrosis and vasculopathy. Using cross-species comparative gene expression profiling we show that murine sclerodematous graft-versus-host disease (sclGVHD) approximates an “inflammatory” subset of human scleroderma and that both diseases demonstrate activation of the IL13 cytokine pathway. We report that both host myeloid cells expressing type I and II activated macrophage markers and graft T-cells produce IL13 and that host mice deficient in either IL13 or IL4Ra, an IL13 signal transducer, are protected from disease. This signaling pathway converges on a single gene, CCL2, which is coordinately upregulated in sclGVHD, in the human inflammatory scleroderma subset and in IL13 treated human dermal fibroblasts. Accordingly, treatment with antibodies to CCL2, and its murine homolog CCL12, prevent sclGVHD. Lastly, we provide evidence that IL13 pathway activation in early scleroderma patients correlates with modified Rodnan skin scores (mRSS). These data indicate that an inflammatory subset of scleroderma is driven by IL13 and may benefit from IL13 or CCL2 blockade. sample vs reference. Total RNA isolated from a time course of primary adult dermal fibroblasts treated with 50nM recombinant IL13 over 24 hours
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Project description:Rationale: Mast cells (MCs) within the airway epithelium in asthma are closely related to airway dysfunction, but crosstalk between airway epithelial cells (AECs) and MCs in asthma remains incompletely understood. Human rhinovirus (HRV) infections are key triggers for asthma progression and AECs from individuals with asthma may have dysregulated anti-viral responses. Objectives: We utilize primary phenotyped AECs in an ex vivo coculture model system to examine crosstalk between AECs and MCs following epithelial HRV infection. Methods: Primary AECs were obtained from children with asthma (n=11) and healthy children (n=10), differentiated at air-liquid interface, and cultured in the presence of laboratory of allergic diseases-2 (LAD2) MCs. AECs were infected with HRV serogroup A 16 (HRV16) for 48 hours. RNA isolated from both AECs and MCs underwent RNA-sequencing (RNAseq) analysis. Direct effects of epithelial-derived interferons on LAD2 MCs were examined by qPCR. Results: MCs increased expression of pro-inflammatory and anti-viral genes in AECs. AECs demonstrated a robust antiviral response following HRV16 infection that resulted in significant changes in MC gene expression, including upregulation of genes involved in anti-viral responses, leukocyte activation, and type-2 (T2) inflammation. Subsequent ex vivo modeling demonstrated that IFN-β induces MC IL13 expression. The effects of AEC phenotype were small relative to the effects of viral infection and the presence of MCs. Conclusions: There is significant crosstalk between AECs and MCs, which are present in the epithelium in asthma. Epithelial-derived interferons not only play a role in viral suppression, but further alter MC immune responses including specific T2 genes.
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2011-06-30 | E-GEOD-17914 | biostudies-arrayexpress
Project description:Scleroderma is a lethal and currently irreversible autoimmune disease characterized by widespread tissue fibrosis and vasculopathy. Using cross-species comparative gene expression profiling we show that murine sclerodematous graft-versus-host disease (sclGVHD) approximates an “inflammatory” subset of human scleroderma and that both diseases demonstrate activation of the IL13 cytokine pathway. We report that both host myeloid cells expressing type I and II activated macrophage markers and graft T-cells produce IL13 and that host mice deficient in either IL13 or IL4Rα, an IL13 signal transducer, are protected from disease. This signaling pathway converges on a single gene, CCL2, which is coordinately upregulated in sclGVHD, in the human inflammatory scleroderma subset and in IL13 treated human dermal fibroblasts. Accordingly, treatment with antibodies to CCL2, and its murine homolog CCL12, prevent sclGVHD. Lastly, we provide evidence that IL13 pathway activation in early scleroderma patients correlates with modified Rodnan skin scores (mRSS). These data indicate that an inflammatory subset of scleroderma is driven by IL13 and may benefit from IL13 or CCL2 blockade.
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