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Sputum microRNA‐screening reveals Prostaglandin EP3 receptor as selective target in allergen‐specific immunotherapy

ABSTRACT: Sputum microRNA‐screening reveals Prostaglandin EP3 receptor as selective target in allergen‐specific immunotherapy

PROVIDER: PRJNA764257 | ENA |

REPOSITORIES: ENA

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Sputum microRNA‐screening reveals Prostaglandin EP3 receptor as selective target in allergen‐specific immunotherapy

Project description:Several microRNAs (miRs) have been described as potential biomarkers in liquid biopsies and in the context of allergic asthma, while therapeutic effects on the airway expression of miRs remain elusive. In this study, we investigated epigenetic miR-associated mechanisms in the sputum of grass pollen allergic patients with and without allergen specific immunotherapy (AIT). Induced sputum samples of healthy controls (HC), AIT treated and untreated grass pollen allergic rhinitis patients with (AA) and without asthma (AR) were profiled using miR microarray and transcriptome microarray analysis of the same samples. miR targets were predicted in silico and used to identify inverse regulation. Local PGE2 levels were measured using ELISA. Two Hundred and fifty nine miRs were upregulated in the sputum of AA patients compared with HC, while only one was downregulated. The inverse picture was observed in induced sputum of AIT-treated patients: while 21 miRs were downregulated, only 4 miRs were upregulated in asthmatics upon AIT. Of these 4 miRs, miR3935 stood out, as its predicted target PTGER3, the prostaglandin EP3 receptor, was downregulated in treated AA patients compared with untreated. The levels of its ligand PGE2 in the sputum supernatants of these samples were increased in allergic patients, especially asthmatics, and downregulated after AIT. Finally, local PGE2 levels correlated with ILC2 frequencies, secreted sputum IL13 levels, inflammatory cell load, sputum eosinophils and symptom burden.While profiling the sputum of allergic patients for novel miR expression patterns, we uncovered an association between miR3935 and its predicted target gene, the prostaglandin E3 receptor, which might mediate AIT effects through suppression of the PGE2-PTGER3 axis.

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Project description:Sputum cells collected before (visit 2) and after (visit 4) allergen challenge in asthma patients were isolated and RNA purified for analysis on gene expression arrays. Human subject recruitment part of NIH sponsored protocol as part of the Eosinophil Program Project Grant (PI: Dr. Nizar Jarjour) Sputum cell RNA collected from induced sputum cells before and 48 hours after whole-lung allergen challenge.

2013-04-20 | E-GEOD-46238 | biostudies-arrayexpress

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Allergen-specific immunotherapy induces the suppressive secretoglobin 1A1 in cells of the lower airways

Project description:While several systemic immunomodulatory effects of allergen-specific immunotherapy (AIT) have been discovered, local anti-inflammatory mechanisms in the respiratory tract are largely unknown. We sought to elucidate local and epithelial mechanisms underlying allergen-specific immunotherapy in a genome-wide approach. We induced sputum in hay fever patients and healthy controls during the pollen peak season and stratified patients by effective allergen-immunotherapy or as untreated. Sputum was directly processed after induction and subjected to whole transcriptome RNA microarray analysis. Nasal secretions were analyzed for Secretoglobin1A1 (SCGB1A1) and IL-24 protein levels in an additional validation cohort at three defined time points during the three-year course of AIT. Subsequently, RNA was extracted and subjected to an array-based whole transcriptome analysis. AIT inhibited pro-inflammatory CXCL8, IL24 and CCL26 mRNA expression, while SCGB1A1, IL7, CCL5, CCL23 and WNT5B mRNAs were induced independently of the asthma status and allergen season. In our validation cohort, local increase of SCGB1A1 occurred concomitantly with the reduction of local IL-24 in upper airways during the course of AIT. Additionally, SCGB1A1 was identified as a suppressor of epithelial gene expression.AIT induces a yet unknown local gene expression footprint in the lower airways that on one hand appears to be a result of multiple regulatory pathways and on the other hand reveals SCGB1A1 as novel anti-inflammatory mediator of long-term allergen specific therapeutic intervention in the local environment.

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Project description:The transition from β-cell compensation to β-cell failure is not well understood. Previous works by our group and others have demonstrated a role for Prostaglandin EP3 receptor (EP3), encoded by the Ptger3 gene, in the loss of functional β-cell mass in T2D. The primary endogenous EP3 ligand is the arachidonic acid metabolite, prostaglandin E2 (PGE2). Pancreatic islet EP3 expression, expression of PGE2 synthetic enzymes, and/or PGE2 excretion itself have all been shown as up-regulated in primary mouse and human islets isolated from animals or human organ donors with established T2D as compared to non-diabetic controls. In this study, we took advantage of a rare and fleeting phenotype in which a subset of Black and Tan BRachyury (BTBR) mice homozygous for the Leptinob/ob mutation—a strong genetic model of T2D—were entirely protected from fasting hyperglycemia even with equal obesity and insulin resistance as their hyperglycemic littermates. Utilizing this model, we found numerous alterations in full-body metabolic parameters in T2D-protected mice (e.g., gut microbiome composition, circulating pancreatic and incretin hormones, and markers of systemic inflammation) that correlate with improvements in EP3-mediated β-cell dysfunction.

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