Summary of Study ST002438

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 PR001570. The data can be accessed directly via it's Project DOI: 10.21228/M8RM66 This work is supported by NIH grant, U2C- DK119886.

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This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002438
Study TitleOzone alters glycosphingolipid metabolism and exacerbates characteristics of asthma in mice
Study SummaryAsthma is a common chronic respiratory disease exacerbated by multiple environmental factors, including exposure to air pollutants such as ozone. Acute ozone exposure has previously been implicated in airway inflammation, airway hyperreactivity, and other characteristics of asthma. Altered sphingolipid metabolism following ozone exposure may contribute to the molecular mechanisms underlying these previously reported effects. This study aimed to identify changes in metabolomic profiles and characteristics of asthma in allergen-sensitized mice following ozone exposure to provide insights regarding mechanisms of ozone-induced exacerbations in asthma. Adult male and female BALB/c mice were sensitized intranasally to house dust mite allergen (HDM) on days 1, 3, and 5 followed by HDM challenge on days 12-14. Mice were subsequently exposed to ozone following each HDM challenge for 6 hr/day. Bronchoalveolar lavage, plasma, whole lung lobes, and microdissected lung airways were collected from 8 female and 8 male mice for metabolomics analysis. 6 female and 6 male mice underwent methacholine challenge using a forced oscillation technique to assess pulmonary function. HDM-sensitized male mice exposed to ozone displayed synergistically increased airway hyperreactivity as well as increased airway inflammation and eosinophilia relative to control mice. Effects in male mice were significantly more severe than the effects observed in females. Both HDM-sensitized male and female mice exposed to ozone displayed significant decreases in multiple classes of sphingolipids in microdissected airways. However, glycosphingolipids were significantly increased in females and to a lesser extent in males. These results potentially implicate glycosphingolipids in protecting against severe outcomes of ozone exposure that coincide with exacerbation of allergic asthma.
Institute
University of California, Davis
Last NameStevens
First NameNathanial
Address451 Health Sciences Drive
Emailncstevens@ucdavis.edu
Phone8282844315
Submit Date2022-08-25
Raw Data AvailableYes
Raw Data File Type(s)raw(Thermo)
Analysis Type DetailLC-MS
Release Date2023-01-25
Release Version1
Nathanial Stevens Nathanial Stevens
https://dx.doi.org/10.21228/M8RM66
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR001570
Project DOI:doi: 10.21228/M8RM66
Project Title:Ozone alters glycosphingolipid metabolism and exacerbates characteristics of asthma in mice
Project Summary:Asthma is a common chronic respiratory disease exacerbated by multiple environmental factors, including exposure to air pollutants such as ozone. Acute ozone exposure has previously been implicated in airway inflammation, airway hyperreactivity, and other characteristics of asthma. Altered sphingolipid metabolism following ozone exposure may contribute to the molecular mechanisms underlying these previously reported effects. This study aimed to identify changes in metabolomic profiles and characteristics of asthma in allergen-sensitized mice following ozone exposure to provide insights regarding mechanisms of ozone-induced exacerbations in asthma. Adult male and female BALB/c mice were sensitized intranasally to house dust mite allergen (HDM) on days 1, 3, and 5 followed by HDM challenge on days 12-14. Mice were subsequently exposed to ozone following each HDM challenge for 6 hr/day. Bronchoalveolar lavage, plasma, whole lung lobes, and microdissected lung airways were collected from 8 female and 8 male mice for metabolomics analysis. 6 female and 6 male mice underwent methacholine challenge using a forced oscillation technique to assess pulmonary function. HDM-sensitized male mice exposed to ozone displayed synergistically increased airway hyperreactivity as well as increased airway inflammation and eosinophilia relative to control mice. Effects in male mice were significantly more severe than the effects observed in females. Both HDM-sensitized male and female mice exposed to ozone displayed significant decreases in multiple classes of sphingolipids in microdissected airways. However, glycosphingolipids were significantly increased in females and to a lesser extent in males. These results potentially implicate glycosphingolipids in protecting against severe outcomes of ozone exposure that coincide with exacerbation of allergic asthma.
Institute:University of California Davis
Last Name:Stevens
First Name:Nathanial
Address:451 Health Sciences Drive, Davis, CA, 95616, USA
Email:ncstevens@ucdavis.edu
Phone:8282844315
Funding Source:R21 ES030276, T32 ES007059, T32 HL007013, NIH U19 AG023122
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