Summary of project PR000655

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000655. The data can be accessed directly via it's Project DOI: 10.21228/M80X1K This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR000655
Project DOI:doi: 10.21228/M80X1K
Project Title:Explore Metabolites and Pathways Associated Increased Airway Hyperresponsiveness in Asthma
Project Type:Open-label, prospective corhort study
Project Summary:Asthma is a heterogeneous disease largely defined by chronic airway inflammation with similar symptomatology in patients that includes wheezing, shortness of breath, chest tightness and cough. However, underlying these common symptoms are varying endotypes with distinct pathophysiological processes. Metabolomic studies in patients with asthma are emerging and suggest that metabolomics can characterize distinct asthma phenotypes. In a completed study, we identified a population of patients with asthma who have increased airway hyperresponsiveness (airway hyperresponsiveness is a marker for asthma disease severity) who are characterized by race (African American) and genotype (ADRB2 Arg16/Arg) compared with patients who have less airway hyperresponsiveness (African Americans and whites with differing ADRB2 genotypes). This group may represent a distinct endotype of asthma with unique metabolomic and lipidomic characteristics. The aims of this project are to (1) use metabolomic and lipidomic analysis to identify metabolites present in plasma in this population of patients with asthma who have increased airway hyperresponsiveness (African Americans who carry the ADRB2 Arg16/Arg genotype) and patients with asthma who have less airway hyperresponsiveness (African Americans and whites with differing ADRB2 genotypes); and (2) identify pathways that will improve the understanding of increased airway hyperresponsiveness in this population. We hypothesize that there will be unique metabolic pathways in the population with increased airway hyperresponsiveness that will be distinct from pathways in patients with lower airway hyperresponsiveness. In this project will use data and samples that were previously collected as part of the NIH funded project “Pharmacogenetics of β2-Agonists in Asthma” (Blake, PI K23 HL081245). Blood was collected in 55 African Americans and whites after receiving 2-weeks treatment with inhaled fluticasone. Samples were stored on ice until processed and plasma frozen at -80°C. If our findings indicate distinct metabolic pathways are present using global metabolomic and lipodomic analysis, we will seek to replicate our findings using samples and data from phenotypically well characterized participants who participated in trials conducted through the American Lung Association Airways Clinical Research Centers network, of which Nemours has been a highly productive site since 1999. Future controlled trials would be conducted to evaluate treatments based upon molecular pathways identified through metabolomic and lipidomic analysis.
Institute:Nemours Children's Specialty Care
Department:Center for Pharmacogenomics and Translational Research
Laboratory:Pulmonology laboratory
Last Name:Blake
First Name:Kathryn
Address:807 Childrens's Way Jacksonville, Florida 32207
Email:Kathryn.Blake@nemours.org
Phone:(904) 697-3806
Funding Source:SECIM pilot and feasibility, NIH U24 DK097209

Summary of all studies in project PR000655

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)		 Release
Date		VersionSamplesDownload
(* : Contains raw data)
ST000954 Explore Metabolites and Pathways Associated Increased Airway Hyperresponsiveness in Asthma Homo sapiens University of Florida MS* 2021-01-19 1 55 Uploaded data (32.3G)*
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