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                    <forename type="first">Thomas</forename>
                    <surname>Geiser</surname>
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                    <forename type="first">Jacek</forename>
                    <surname>Musial</surname>
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                  <persName>
                    <forename type="first">Dominick</forename>
                    <surname>Shaw</surname>
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                  <idno type="idhal" notation="numeric">793662</idno>
                  <idno type="halauthorid" notation="string">1491621-793662</idno>
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                    <forename type="first">Barbro</forename>
                    <surname>Dahlén</surname>
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                    <forename type="first">Sile</forename>
                    <surname>Hu</surname>
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                  <persName>
                    <forename type="first">Jessica</forename>
                    <surname>Lasky-Su</surname>
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                    <forename type="first">Peter</forename>
                    <surname>Sterk</surname>
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                    <forename type="first">Kian Fan</forename>
                    <surname>Chung</surname>
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                    <forename type="first">Ratko</forename>
                    <surname>Djukanovic</surname>
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                    <forename type="first">Sven-Erik</forename>
                    <surname>Dahlén</surname>
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                    <forename type="first">Ian</forename>
                    <surname>Adcock</surname>
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                  <persName>
                    <forename type="first">Craig</forename>
                    <surname>Wheelock</surname>
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                  <idno type="idhal" notation="numeric">800603</idno>
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                <idno type="halJournalId" status="VALID">13128</idno>
                <idno type="issn">0903-1936</idno>
                <idno type="eissn">1399-3003</idno>
                <title level="j">European Respiratory Journal</title>
                <imprint>
                  <publisher>European Respiratory Society</publisher>
                  <biblScope unit="pp">2101733</biblScope>
                  <date type="datePub">2021-11-25</date>
                </imprint>
              </monogr>
              <idno type="doi">10.1183/13993003.01733-2021</idno>
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              <classCode scheme="halTreeTypology" n="ART">Journal articles</classCode>
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            <abstract xml:lang="en">
              <p>Introduction Asthma is a heterogeneous disease with poorly defined phenotypes. Severe asthmatics often receive multiple treatments including oral corticosteroids (OCS). Treatment may modify the observed metabotype, rendering it challenging to investigate underlying disease mechanisms. Here, we aimed to identify dysregulated metabolic processes in relation to asthma severity and medication. Methods Baseline urine was collected prospectively from healthy participants (n=100), mild-to-moderate asthmatics (n=87) and severe asthmatics (n=418) in the cross-sectional U-BIOPRED cohort; 12–18-month longitudinal samples were collected from severe asthmatics (n=305). Metabolomics data were acquired using high-resolution mass spectrometry and analysed using univariate and multivariate methods. Results Ninety metabolites were identified, with 40 significantly altered (p&lt;0.05, FDR&lt;0.05) in severe asthma and 23 by OCS use. Multivariate modelling showed that observed metabotypes in healthy participants and mild-to-moderate asthmatics differed significantly from severe asthmatics (p=2.6×10 −20 ), OCS-treated asthmatics differed significantly from non-treated (p=9.5×10 −4 ), and longitudinal metabotypes demonstrated temporal stability. Carnitine levels evidenced the strongest OCS-independent decrease in severe asthma. Reduced carnitine levels were associated with mitochondrial dysfunction via decreases in pathway enrichment scores of fatty acid metabolism and reduced expression of the carnitine transporter SLC22A5 in sputum and bronchial brushings. Conclusions This is the first large-scale study to delineate disease- and OCS-associated metabolic differences in asthma. The widespread associations with different therapies upon the observed metabotypes demonstrate the necessity to evaluate potential modulating effects on a treatment- and metabolite-specific basis. Altered carnitine metabolism is a potentially actionable therapeutic target that is independent of OCS treatment, highlighting the role of mitochondrial dysfunction in severe asthma.</p>
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          <date type="start">2020-01-01</date>
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              <addrLine>Faculté de Médecine de la Timone 27 boulevard Jean Moulin 13385 MARSEILLE CEDEX 5</addrLine>
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