Metabolic pathways of lung inflammation revealed by high-resolution metabolomics (HRM) of H1N1 influenza virus infection in mice.
Identifieur interne : 000B71 ( Main/Exploration ); précédent : 000B70; suivant : 000B72Metabolic pathways of lung inflammation revealed by high-resolution metabolomics (HRM) of H1N1 influenza virus infection in mice.
Auteurs : Joshua D. Chandler ; Xin Hu ; Eun-Ju Ko [Géorgie (pays)] ; Soojin Park [Géorgie (pays)] ; Young-Tae Lee [Géorgie (pays)] ; Michael Orr ; Jolyn Fernandes ; Karan Uppal ; Sang-Moo Kang [Géorgie (pays)] ; Dean P. Jones ; Young-Mi Go [États-Unis]Source :
- American journal of physiology. Regulatory, integrative and comparative physiology [ 1522-1490 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Femelle, Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (virologie), Mâle, Métabolome (immunologie), Métabolomique, Pneumopathie virale (immunologie), Pneumopathie virale (virologie), Poumon (immunologie), Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A, Tests de criblage à haut débit, Voies et réseaux métaboliques (immunologie).
- MESH :
- immunologie : Infections à Orthomyxoviridae, Métabolome, Pneumopathie virale, Poumon, Voies et réseaux métaboliques.
- virologie : Infections à Orthomyxoviridae, Pneumopathie virale.
- Animaux, Femelle, Mâle, Métabolomique, Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A, Tests de criblage à haut débit.
English descriptors
- KwdEn :
- Animals, Female, High-Throughput Screening Assays, Influenza A Virus, H1N1 Subtype, Lung (immunology), Male, Metabolic Networks and Pathways (immunology), Metabolome (immunology), Metabolomics, Mice, Mice, Inbred C57BL, Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (virology), Pneumonia, Viral (immunology), Pneumonia, Viral (virology).
- MESH :
Abstract
Influenza is a significant health concern worldwide. Viral infection induces local and systemic activation of the immune system causing attendant changes in metabolism. High-resolution metabolomics (HRM) uses advanced mass spectrometry and computational methods to measure thousands of metabolites inclusive of most metabolic pathways. We used HRM to identify metabolic pathways and clusters of association related to inflammatory cytokines in lungs of mice with H1N1 influenza virus infection. Infected mice showed progressive weight loss, decreased lung function, and severe lung inflammation with elevated cytokines [interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ] and increased oxidative stress via cysteine oxidation. HRM showed prominent effects of influenza virus infection on tryptophan and other amino acids, and widespread effects on pathways including purines, pyrimidines, fatty acids, and glycerophospholipids. A metabolome-wide association study (MWAS) of the aforementioned inflammatory cytokines was used to determine the relationship of metabolic responses to inflammation during infection. This cytokine-MWAS (cMWAS) showed that metabolic associations consisted of distinct and shared clusters of 396 metabolites highly correlated with inflammatory cytokines. Strong negative associations of selected glycosphingolipid, linoleate, and tryptophan metabolites with IFN-γ contrasted strong positive associations of glycosphingolipid and bile acid metabolites with IL-1β, TNF-α, and IL-10. Anti-inflammatory cytokine IL-10 had strong positive associations with vitamin D, purine, and vitamin E metabolism. The detailed metabolic interactions with cytokines indicate that targeted metabolic interventions may be useful during life-threatening crises related to severe acute infection and inflammation.
DOI: 10.1152/ajpregu.00298.2016
PubMed: 27558316
Affiliations:
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Le document en format XML
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Chandler</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Hu, Xin" sort="Hu, Xin" uniqKey="Hu X" first="Xin" last="Hu">Xin Hu</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Ko, Eun Ju" sort="Ko, Eun Ju" uniqKey="Ko E" first="Eun-Ju" last="Ko">Eun-Ju Ko</name><affiliation wicri:level="1"><nlm:affiliation>Georgia State University, Atlanta, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Georgia State University, Atlanta</wicri:regionArea><wicri:noRegion>Atlanta</wicri:noRegion></affiliation></author><author><name sortKey="Park, Soojin" sort="Park, Soojin" uniqKey="Park S" first="Soojin" last="Park">Soojin Park</name><affiliation wicri:level="1"><nlm:affiliation>Georgia State University, Atlanta, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Georgia State University, Atlanta</wicri:regionArea><wicri:noRegion>Atlanta</wicri:noRegion></affiliation></author><author><name sortKey="Lee, Young Tae" sort="Lee, Young Tae" uniqKey="Lee Y" first="Young-Tae" last="Lee">Young-Tae Lee</name><affiliation wicri:level="1"><nlm:affiliation>Georgia State University, Atlanta, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Georgia State University, Atlanta</wicri:regionArea><wicri:noRegion>Atlanta</wicri:noRegion></affiliation></author><author><name sortKey="Orr, Michael" sort="Orr, Michael" uniqKey="Orr M" first="Michael" last="Orr">Michael Orr</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Fernandes, Jolyn" sort="Fernandes, Jolyn" uniqKey="Fernandes J" first="Jolyn" last="Fernandes">Jolyn Fernandes</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Uppal, Karan" sort="Uppal, Karan" uniqKey="Uppal K" first="Karan" last="Uppal">Karan Uppal</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Kang, Sang Moo" sort="Kang, Sang Moo" uniqKey="Kang S" first="Sang-Moo" last="Kang">Sang-Moo Kang</name><affiliation wicri:level="1"><nlm:affiliation>Georgia State University, Atlanta, Georgia.</nlm:affiliation><country xml:lang="fr">Géorgie (pays)</country><wicri:regionArea>Georgia State University, Atlanta</wicri:regionArea><wicri:noRegion>Atlanta</wicri:noRegion></affiliation></author><author><name sortKey="Jones, Dean P" sort="Jones, Dean P" uniqKey="Jones D" first="Dean P" last="Jones">Dean P. Jones</name><affiliation><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and.</nlm:affiliation><wicri:noCountry code="subField">Georgia; and</wicri:noCountry></affiliation></author><author><name sortKey="Go, Young Mi" sort="Go, Young Mi" uniqKey="Go Y" first="Young-Mi" last="Go">Young-Mi Go</name><affiliation wicri:level="1"><nlm:affiliation>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta, Georgia; and ygo@emory.edu.</nlm:affiliation><country wicri:rule="url">États-Unis</country><wicri:regionArea>Division of Pulmonary Medicine, Department of Medicine, Emory University, Atlanta</wicri:regionArea><wicri:noRegion>Atlanta</wicri:noRegion></affiliation></author></analytic><series><title level="j">American journal of physiology. Regulatory, integrative and comparative physiology</title><idno type="eISSN">1522-1490</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Female</term><term>High-Throughput Screening Assays</term><term>Influenza A Virus, H1N1 Subtype</term><term>Lung (immunology)</term><term>Male</term><term>Metabolic Networks and Pathways (immunology)</term><term>Metabolome (immunology)</term><term>Metabolomics</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Orthomyxoviridae Infections (immunology)</term><term>Orthomyxoviridae Infections (virology)</term><term>Pneumonia, Viral (immunology)</term><term>Pneumonia, Viral (virology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Infections à Orthomyxoviridae (immunologie)</term><term>Infections à Orthomyxoviridae (virologie)</term><term>Mâle</term><term>Métabolome (immunologie)</term><term>Métabolomique</term><term>Pneumopathie virale (immunologie)</term><term>Pneumopathie virale (virologie)</term><term>Poumon (immunologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Sous-type H1N1 du virus de la grippe A</term><term>Tests de criblage à haut débit</term><term>Voies et réseaux métaboliques (immunologie)</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Métabolome</term><term>Pneumopathie virale</term><term>Poumon</term><term>Voies et réseaux métaboliques</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Lung</term><term>Metabolic Networks and Pathways</term><term>Metabolome</term><term>Orthomyxoviridae Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Orthomyxoviridae Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>High-Throughput Screening Assays</term><term>Influenza A Virus, H1N1 Subtype</term><term>Male</term><term>Metabolomics</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Mâle</term><term>Métabolomique</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Sous-type H1N1 du virus de la grippe A</term><term>Tests de criblage à haut débit</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza is a significant health concern worldwide. Viral infection induces local and systemic activation of the immune system causing attendant changes in metabolism. High-resolution metabolomics (HRM) uses advanced mass spectrometry and computational methods to measure thousands of metabolites inclusive of most metabolic pathways. We used HRM to identify metabolic pathways and clusters of association related to inflammatory cytokines in lungs of mice with H1N1 influenza virus infection. Infected mice showed progressive weight loss, decreased lung function, and severe lung inflammation with elevated cytokines [interleukin (IL)-1β, IL-6, IL-10, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ] and increased oxidative stress via cysteine oxidation. HRM showed prominent effects of influenza virus infection on tryptophan and other amino acids, and widespread effects on pathways including purines, pyrimidines, fatty acids, and glycerophospholipids. A metabolome-wide association study (MWAS) of the aforementioned inflammatory cytokines was used to determine the relationship of metabolic responses to inflammation during infection. This cytokine-MWAS (cMWAS) showed that metabolic associations consisted of distinct and shared clusters of 396 metabolites highly correlated with inflammatory cytokines. Strong negative associations of selected glycosphingolipid, linoleate, and tryptophan metabolites with IFN-γ contrasted strong positive associations of glycosphingolipid and bile acid metabolites with IL-1β, TNF-α, and IL-10. Anti-inflammatory cytokine IL-10 had strong positive associations with vitamin D, purine, and vitamin E metabolism. The detailed metabolic interactions with cytokines indicate that targeted metabolic interventions may be useful during life-threatening crises related to severe acute infection and inflammation.</div></front></TEI><affiliations><list><country><li>Géorgie (pays)</li><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Chandler, Joshua D" sort="Chandler, Joshua D" uniqKey="Chandler J" first="Joshua D" last="Chandler">Joshua D. Chandler</name><name sortKey="Fernandes, Jolyn" sort="Fernandes, Jolyn" uniqKey="Fernandes J" first="Jolyn" last="Fernandes">Jolyn Fernandes</name><name sortKey="Hu, Xin" sort="Hu, Xin" uniqKey="Hu X" first="Xin" last="Hu">Xin Hu</name><name sortKey="Jones, Dean P" sort="Jones, Dean P" uniqKey="Jones D" first="Dean P" last="Jones">Dean P. Jones</name><name sortKey="Orr, Michael" sort="Orr, Michael" uniqKey="Orr M" first="Michael" last="Orr">Michael Orr</name><name sortKey="Uppal, Karan" sort="Uppal, Karan" uniqKey="Uppal K" first="Karan" last="Uppal">Karan Uppal</name></noCountry><country name="Géorgie (pays)"><noRegion><name sortKey="Ko, Eun Ju" sort="Ko, Eun Ju" uniqKey="Ko E" first="Eun-Ju" last="Ko">Eun-Ju Ko</name></noRegion><name sortKey="Kang, Sang Moo" sort="Kang, Sang Moo" uniqKey="Kang S" first="Sang-Moo" last="Kang">Sang-Moo Kang</name><name sortKey="Lee, Young Tae" sort="Lee, Young Tae" uniqKey="Lee Y" first="Young-Tae" last="Lee">Young-Tae Lee</name><name sortKey="Park, Soojin" sort="Park, Soojin" uniqKey="Park S" first="Soojin" last="Park">Soojin Park</name></country><country name="États-Unis"><noRegion><name sortKey="Go, Young Mi" sort="Go, Young Mi" uniqKey="Go Y" first="Young-Mi" last="Go">Young-Mi Go</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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