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dc.contributor.authorCui, Liang
dc.contributor.authorZheng, Dahai
dc.contributor.authorLee, Yie Hou
dc.contributor.authorChan, Tze Khee
dc.contributor.authorKumar, Yadunanda
dc.contributor.authorHo, Wanxing Eugene
dc.contributor.authorOng, Choon Nam
dc.contributor.authorChen, Jianzhu
dc.contributor.authorTannenbaum, Steven R
dc.date.accessioned2017-05-24T19:33:46Z
dc.date.available2017-05-24T19:33:46Z
dc.date.issued2016-05
dc.date.submitted2015-12
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/1721.1/109325
dc.description.abstractInfluenza virus infection (IVI) can cause primary viral pneumonia, which may progress to acute lung injury (ALI) and respiratory failure with a potentially fatal outcome. At present, the interactions between host and influenza virus at molecular levels and the underlying mechanisms that give rise to IVI-induced ALI are poorly understood. We conducted a comprehensive mass spectrometry-based metabolic profiling of serum, lung tissue and bronchoalveolar lavage fluid (BALF) from a non-lethal mouse model with influenza A virus at 0, 6, 10, 14, 21 and 28 days post infection (dpi), representing the major stages of IVI. Distinct metabolite signatures were observed in mice sera, lung tissues and BALF, indicating the molecular differences between systematic and localized host responses to IVI. More than 100 differential metabolites were captured in mice sera, lung tissues and BALF, including purines, pyrimidines, acylcarnitines, fatty acids, amino acids, glucocorticoids, sphingolipids, phospholipids, etc. Many of these metabolites belonged to pulmonary surfactants, indicating IVI-induced aberrations of the pulmonary surfactant system might play an important role in the etiology of respiratory failure and repair. Our findings revealed dynamic host responses to IVI and various metabolic pathways linked to disease progression, and provided mechanistic insights into IVI-induced ALI and repair process.en_US
dc.description.sponsorshipNational Science Foundation (U.S.)en_US
dc.description.sponsorshipSingapore-MIT Alliance for Research and Technology (SMART)en_US
dc.language.isoen_US
dc.publisherSpringer Natureen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/srep26076en_US
dc.rightsCreative Commons Attribution 4.0 International Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.sourceScientific Reportsen_US
dc.titleMetabolomics Investigation Reveals Metabolite Mediators Associated with Acute Lung Injury and Repair in a Murine Model of Influenza Pneumoniaen_US
dc.typeArticleen_US
dc.identifier.citationCui, Liang, Dahai Zheng, Yie Hou Lee, Tze Khee Chan, Yadunanda Kumar, Wanxing Eugene Ho, Jian Zhu Chen, Steven R. Tannenbaum, and Choon Nam Ong. “Metabolomics Investigation Reveals Metabolite Mediators Associated with Acute Lung Injury and Repair in a Murine Model of Influenza Pneumonia.” Scientific Reports 6 (May 18, 2016): 26076.en_US
dc.contributor.departmentDavid H. Koch Institute for Integrative Cancer Research at MITen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Chemistryen_US
dc.contributor.mitauthorChen, Jianzhu
dc.contributor.mitauthorTannenbaum, Steven R
dc.relation.journalScientific Reportsen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsCui, Liang; Zheng, Dahai; Lee, Yie Hou; Chan, Tze Khee; Kumar, Yadunanda; Ho, Wanxing Eugene; Chen, Jian Zhu; Tannenbaum, Steven R.; Ong, Choon Namen_US
dspace.embargo.termsNen_US
dc.identifier.orcidhttps://orcid.org/0000-0002-5687-6154
mit.licensePUBLISHER_CCen_US


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