Inflammation-associated microbiota in pediatric eosinophilic esophagitis
Identifieur interne : 001044 ( Main/Exploration ); précédent : 001043; suivant : 001045Inflammation-associated microbiota in pediatric eosinophilic esophagitis
Auteurs : Alain J. Benitez [États-Unis] ; Christian Hoffmann [États-Unis, Brésil] ; Amanda B. Muir [États-Unis] ; Kara K. Dods [États-Unis] ; Jonathan M. Spergel [États-Unis] ; Frederic D. Bushman [États-Unis] ; Mei-Lun Wang [États-Unis]Source :
- Microbiome [ 2049-2618 ] ; 2015.
Abstract
Eosinophilic esophagitis (EoE) is an allergic disorder characterized by eosinophil-predominant esophageal inflammation, which can be ameliorated by food antigen restriction. Though recent studies suggest that changes in dietary composition may alter the distal gut microbiome, little is currently known about the impact of a restricted diet upon microbial communities of the oral and esophageal microenvironments in the context of EoE. We hypothesize that the oral and esophageal microbiomes of EoE patients are distinct from non-EoE controls, that these differences correspond to changes in esophageal inflammation, and that targeted therapeutic dietary intervention may influence community structure. Using 16S rRNA gene sequencing, we characterized the bacterial composition of the oral and esophageal microenvironments using oral swabs and esophageal biopsies from 35 non-EoE pediatric controls and compared this cohort to samples from 33 pediatric EoE subjects studied in a longitudinal fashion before and after defined dietary changes.
Firmicutes were more abundant in esophageal samples compared to oral. Proportions of bacterial communities were significantly different comparing all EoE esophageal microbiota to non-EoE controls, with enrichment of Proteobacteria, including
In conclusion, the esophageal microbiome in EoE is distinct from that of non-EoE controls, with maximal differences observed during active allergic inflammation.
The online version of this article (doi:10.1186/s40168-015-0085-6) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1186/s40168-015-0085-6
PubMed: 26034601
PubMed Central: 4450515
Affiliations:
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Dods</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Division of Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia, PA 19104 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Division of Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia</wicri:cityArea></affiliation></author><author><name sortKey="Spergel, Jonathan M" sort="Spergel, Jonathan M" uniqKey="Spergel J" first="Jonathan M." last="Spergel">Jonathan M. 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Bushman</name><affiliation wicri:level="2"><nlm:aff id="Aff2">Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, 3610 Hamilton Walk, Philadelphia, PA 19104 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Microbiology, Perelman School of Medicine, University of Pennsylvania, 3610 Hamilton Walk, Philadelphia</wicri:cityArea></affiliation></author><author><name sortKey="Wang, Mei Lun" sort="Wang, Mei Lun" uniqKey="Wang M" first="Mei-Lun" last="Wang">Mei-Lun Wang</name><affiliation wicri:level="2"><nlm:aff id="Aff1">Division of Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia, PA 19104 USA</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Division of Gastroenterology, Hepatology, and Nutrition, The Children’s Hospital of Philadelphia, Philadelphia</wicri:cityArea></affiliation><affiliation wicri:level="2"><nlm:aff id="Aff4">Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA USA</nlm:aff><country>États-Unis</country><placeName><region type="state">Pennsylvanie</region></placeName><wicri:cityArea>Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia</wicri:cityArea></affiliation></author></analytic><series><title level="j">Microbiome</title><idno type="eISSN">2049-2618</idno><imprint><date when="2015">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Eosinophilic esophagitis (EoE) is an allergic disorder characterized by eosinophil-predominant esophageal inflammation, which can be ameliorated by food antigen restriction. Though recent studies suggest that changes in dietary composition may alter the distal gut microbiome, little is currently known about the impact of a restricted diet upon microbial communities of the oral and esophageal microenvironments in the context of EoE. We hypothesize that the oral and esophageal microbiomes of EoE patients are distinct from non-EoE controls, that these differences correspond to changes in esophageal inflammation, and that targeted therapeutic dietary intervention may influence community structure. Using 16S rRNA gene sequencing, we characterized the bacterial composition of the oral and esophageal microenvironments using oral swabs and esophageal biopsies from 35 non-EoE pediatric controls and compared this cohort to samples from 33 pediatric EoE subjects studied in a longitudinal fashion before and after defined dietary changes.</p></sec><sec><title>Results</title><p>Firmicutes were more abundant in esophageal samples compared to oral. Proportions of bacterial communities were significantly different comparing all EoE esophageal microbiota to non-EoE controls, with enrichment of Proteobacteria, including <italic>Neisseria</italic> and <italic>Corynebacterium</italic> in the EoE cohort, and predominance of the Firmicutes in non-EoE control subjects. We detected a statistically significant difference between actively inflamed EoE biopsies and non-EoE controls. Overall, though targeted dietary intervention did not lead to significant differences in either oral or esophageal microbiota, reintroduction of highly allergenic foods led to enrichment in <italic>Ganulicatella</italic> and <italic>Campylobacter</italic> genera in the esophagus.</p></sec><sec><title>Conclusions</title><p>In conclusion, the esophageal microbiome in EoE is distinct from that of non-EoE controls, with maximal differences observed during active allergic inflammation.</p></sec><sec><title>Electronic supplementary material</title><p>The online version of this article (doi:10.1186/s40168-015-0085-6) contains supplementary material, which is available to authorized users.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Muir, Ab" uniqKey="Muir A">AB Muir</name></author><author><name sortKey="Lim, Dm" uniqKey="Lim D">DM Lim</name></author><author><name sortKey="Benitez, Aj" uniqKey="Benitez A">AJ Benitez</name></author><author><name sortKey="Modayur Chandramouleeswaran, P" uniqKey="Modayur Chandramouleeswaran P">P Modayur Chandramouleeswaran</name></author><author><name sortKey="Lee, Aj" uniqKey="Lee A">AJ Lee</name></author><author><name sortKey="Ruchelli, Ed" uniqKey="Ruchelli E">ED Ruchelli</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liacouras, Ca" uniqKey="Liacouras C">CA Liacouras</name></author><author><name sortKey="Furuta, Gt" uniqKey="Furuta G">GT Furuta</name></author><author><name sortKey="Hirano, I" uniqKey="Hirano I">I Hirano</name></author><author><name sortKey="Atkins, D" uniqKey="Atkins D">D Atkins</name></author><author><name sortKey="Attwood, Se" uniqKey="Attwood S">SE Attwood</name></author><author><name sortKey="Bonis, Pa" uniqKey="Bonis P">PA Bonis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kelly, Kj" uniqKey="Kelly K">KJ Kelly</name></author><author><name sortKey="Lazenby, Aj" 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Paulo</li></orgName></list><tree><country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Benitez, Alain J" sort="Benitez, Alain J" uniqKey="Benitez A" first="Alain J" last="Benitez">Alain J. Benitez</name></region><name sortKey="Bushman, Frederic D" sort="Bushman, Frederic D" uniqKey="Bushman F" first="Frederic D." last="Bushman">Frederic D. Bushman</name><name sortKey="Dods, Kara K" sort="Dods, Kara K" uniqKey="Dods K" first="Kara K." last="Dods">Kara K. Dods</name><name sortKey="Hoffmann, Christian" sort="Hoffmann, Christian" uniqKey="Hoffmann C" first="Christian" last="Hoffmann">Christian Hoffmann</name><name sortKey="Muir, Amanda B" sort="Muir, Amanda B" uniqKey="Muir A" first="Amanda B." last="Muir">Amanda B. Muir</name><name sortKey="Muir, Amanda B" sort="Muir, Amanda B" uniqKey="Muir A" first="Amanda B." last="Muir">Amanda B. Muir</name><name sortKey="Spergel, Jonathan M" sort="Spergel, Jonathan M" uniqKey="Spergel J" first="Jonathan M." last="Spergel">Jonathan M. Spergel</name><name sortKey="Spergel, Jonathan M" sort="Spergel, Jonathan M" uniqKey="Spergel J" first="Jonathan M." last="Spergel">Jonathan M. Spergel</name><name sortKey="Wang, Mei Lun" sort="Wang, Mei Lun" uniqKey="Wang M" first="Mei-Lun" last="Wang">Mei-Lun Wang</name><name sortKey="Wang, Mei Lun" sort="Wang, Mei Lun" uniqKey="Wang M" first="Mei-Lun" last="Wang">Mei-Lun Wang</name></country><country name="Brésil"><region name="État de São Paulo"><name sortKey="Hoffmann, Christian" sort="Hoffmann, Christian" uniqKey="Hoffmann C" first="Christian" last="Hoffmann">Christian Hoffmann</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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