Summary of Study ST000069

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR000066. The data can be accessed directly via it's Project DOI: 10.21228/M8QG6H This work is supported by NIH grant, U2C- DK119886.


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Study IDST000069
Study TitleMetabolomic profiling of influenza: a 2009 pandemic H1N1 influenza in lean and obese mice (via blood and tissue)
Study SummaryLung samples were obtained at 15 weeks from 56 mice that had received either chow, a low fat diet, or a high fat diet and that were uninfected, 4 days post-infection, or 8 days post-infection.
University of North Carolina
DepartmentSystems and Translational Sciences
LaboratorySumner Lab
Last NameSumner
First NameSusan
AddressEastern Regional Comprehensive Metabolomics Resource Core, UNC Nutrition Research Institute, 500 Laureate Way, Kannapolis, NC, 28081
Submit Date2014-06-14
Num Groups9
Total Subjects55
Raw Data AvailableNo
Raw Data File Type(s)raw(Waters)
Analysis Type DetailLC-MS
Release Date2015-06-01
Release Version1
Susan Sumner Susan Sumner application/zip

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Project ID:PR000066
Project DOI:doi: 10.21228/M8QG6H
Project Title:Metabolomic profiling of influenza: a 2009 pandemic H1N1 influenza in lean and obese mice
Project Type:Effects and role of obesity on the severity of influenza
Project Summary:During the 2009 H1N1 influenza pandemic outbreak, obese individuals were reported to be at greater risk for morbidity and mortality from pandemic infection. However, the mechanisms contributing to greater influenza severity in infected obese individuals remain unclear. Given that one in ten individuals is obese, and worldwide influenza outbreaks are a consistent public health burden, garnering a better understanding of the pathways and mechanisms contributing to greater influenza severity in the obese is essential for limiting influenza infection mortality in this at-risk population. Closely paralleling pH1N1 infection outcome in humans, obese mice exhibit increased morbidity and mortality following pH1N1 infection. In mice, obesity impairs the function of natural killer cells, dendritic cells, macrophage, B cells and memory T cells. Further, several analyses of lung antiviral responses revealed that obese mice have greater lung damage, lung immune cell infiltration and impaired lung healing after infection. Nevertheless, it remains unclear how altered immune cell function contributes to greater lung damage and increased infection severity in obese mice. Metabolomics will be used to dissect the metabolic consequences of obesity on the immune response to pH1N1 infection. We will compare metabolic profiles of lung-specific and peripheral samples from uninfected and infected lean and obese mice during early and late phases of influenza immunity.
Institute:University of North Carolina at Chapel Hill
Department:Department of Nutrition
Last Name:Beck
First Name:Melinda
Address:2303 MHRB, CB #7461, UNC, Chapel Hill NC 27599