Decline in Presumptively Protective Gut Bacterial Species and Metabolites Are Paradoxically Associated with Disease Improvement in Pediatric Crohn’s Disease During Enteral Nutrition

The gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.MethodsFive fecal samples were collected fro...

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Published inInflammatory bowel diseases Vol. 20; no. 5; pp. 861 - 871
Main Authors Gerasimidis, Konstantinos, Bertz, Martin, Hanske, Laura, Junick, Jana, Biskou, Olga, Aguilera, Margarita, Garrick, Vikki, Russell, Richard K., Blaut, Michael, McGrogan, Paraic, Edwards, Christine A.
Format Journal Article
LanguageEnglish
Published Oxford, UK Oxford University Press 01.05.2014
Subjects
Online AccessGet full text
ISSN1078-0998
1536-4844
1536-4844
DOI10.1097/MIB.0000000000000023

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Abstract The gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.MethodsFive fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.ResultsOverall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.ConclusionsEEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
AbstractList The gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.MethodsFive fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.ResultsOverall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.ConclusionsEEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
BackgroundThe gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.MethodsFive fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.ResultsOverall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.ConclusionsEEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
The gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.BACKGROUNDThe gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN.Five fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.METHODSFive fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured.Overall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.RESULTSOverall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet.EEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.CONCLUSIONSEEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
Background: The gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN. Methods: Five fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured. Results: Overall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P [< or =] 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet. Conclusions: EEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
The gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of action remains unknown. This study assessed serial changes in the fecal microbiota milieu during EEN. Five fecal samples were collected from CD children: 4 during EEN (start, 15, 30, end EEN approximately 60 days) and the fifth on habitual diet. Two samples were collected from healthy control subjects. Fecal pH, bacterial metabolites, global microbial diversity abundance, composition stability, and quantitative changes of total and 7 major bacterial groups previously implicated in CD were measured. Overall, 68 samples were from 15 CD children and 40 from 21 control subjects. Fecal pH and total sulfide increased and butyric acid decreased during EEN (all P < 0.05). Global bacterial diversity abundance decreased (P < 0.05); a higher degree of microbiota composition stability was seen in control subjects than in CD children during EEN (at P ≤ 0.008). Faecalibacterium prausnitzii spp concentration significantly decreased after 30 days on EEN (P < 0.05). In patients who responded to EEN, the magnitude of the observed changes was greater and the concentration of Bacteroides/Prevotella group decreased (P < 0.05). All these changes reverted to pretreatment levels on free diet, and EEN microbiota diversity increased when the children returned to their free diet. EEN impacts on gut microbiota composition and changes fecal metabolic activity. It is difficult to infer a causative association between such changes and disease improvement, but the results do challenge the current perception of a protective role for F. prausnitzii in CD.
Author Garrick, Vikki
Bertz, Martin
McGrogan, Paraic
Gerasimidis, Konstantinos
Hanske, Laura
Junick, Jana
Blaut, Michael
Aguilera, Margarita
Russell, Richard K.
Biskou, Olga
Edwards, Christine A.
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  givenname: Konstantinos
  surname: Gerasimidis
  fullname: Gerasimidis, Konstantinos
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
– sequence: 2
  givenname: Martin
  surname: Bertz
  fullname: Bertz, Martin
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
– sequence: 3
  givenname: Laura
  surname: Hanske
  fullname: Hanske, Laura
  organization: ‡Department of Gastrointestinal Microbiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee, Nuthetal, Germany
– sequence: 4
  givenname: Jana
  surname: Junick
  fullname: Junick, Jana
  organization: ‡Department of Gastrointestinal Microbiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee, Nuthetal, Germany
– sequence: 5
  givenname: Olga
  surname: Biskou
  fullname: Biskou, Olga
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
– sequence: 6
  givenname: Margarita
  surname: Aguilera
  fullname: Aguilera, Margarita
  organization: §Department of Microbiology, Faculty of Pharmacy, University of Granada, Campus Universitario de Cartuja, Granada, Spain
– sequence: 7
  givenname: Vikki
  surname: Garrick
  fullname: Garrick, Vikki
  organization: †Department of Pediatric Gastroenterology, Hepatology and Nutrition, National Health Service Scotland, Royal Hospital for Sick Children, Glasgow, United Kingdom
– sequence: 8
  givenname: Richard K.
  surname: Russell
  fullname: Russell, Richard K.
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
– sequence: 9
  givenname: Michael
  surname: Blaut
  fullname: Blaut, Michael
  organization: ‡Department of Gastrointestinal Microbiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Arthur-Scheunert-Allee, Nuthetal, Germany
– sequence: 10
  givenname: Paraic
  surname: McGrogan
  fullname: McGrogan, Paraic
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
– sequence: 11
  givenname: Christine A.
  surname: Edwards
  fullname: Edwards, Christine A.
  organization: Human Nutrition, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24651582$$D View this record in MEDLINE/PubMed
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Cites_doi 10.3109/00365521.2012.703234
10.1016/0167-7012(92)90071-B
10.1073/pnas.0804812105
10.1002/ibd.21916
10.1016/S0899-9007(97)00493-0
10.1053/j.gastro.2007.08.041
10.1136/gut.41.1.77
10.1038/sj.bjp.0707193
10.1097/00005176-199105000-00005
10.1136/gut.52.2.237
10.1371/journal.pone.0057923
10.1053/j.gastro.2006.02.033
10.1111/j.1365-2036.2009.04067.x
10.1136/gut.2006.108449
10.1111/j.1572-0241.2006.01020.x
10.1053/j.gastro.2007.11.059
10.1177/01486071050290S4S173
10.1155/2005/269076
10.1007/s00394-004-0457-3
10.1111/j.1572-0241.1998.083_c.x
10.1023/A:1010661706385
10.1023/A:1018848709769
10.1097/01.MIB.0000200323.38139.c6
10.1371/journal.pone.0058825
10.1136/gut.38.6.870
10.1038/mi.2010.87
10.1079/PNS2003317
10.1016/j.dld.2012.04.014
10.1128/AEM.00508-07
10.1097/MCG.0b013e3181f39af5
10.1017/S0007114510001030
10.1111/apt.12230
10.1002/ibd.20903
10.1136/gut.41.1.70
10.1093/jn/135.8.1896
10.1111/j.1365-2036.2008.03796.x
ContentType Journal Article
Copyright Copyright © 2014 Crohn's & Colitis Foundation of America, Inc. 2014
Copyright © 2014 Crohn's & Colitis Foundation of America, Inc.
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– notice: Copyright © 2014 Crohn's & Colitis Foundation of America, Inc.
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short-chain fatty acids
gut microbiota
pediatrics
Crohn’s disease
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References Benus (R25-10-20140418) 2010; 104
Moore (R29-10-20140418) 1997; 41
Jorgensen (R31-10-20140418) 2001; 46
Sartor (R4-10-20140418) 2008; 134
Geypens (R33-10-20140418) 1997; 41
Whelan (R6-10-20140418) 2004; 63
Strocchi (R17-10-20140418) 1992; 15
Ruemmele (R3-10-20140418) 2000; 136
Sokol (R18-10-20140418) 2006; 12
Shiga (R9-10-20140418) 2012; 44
Gerasimidis (R13-10-20140418) 2012; 18
Seksik (R19-10-20140418) 2003; 52
El (R37-10-20140418) 1996; 38
Hyams (R15-10-20140418) 1991; 12
Santhanam (R26-10-20140418) 2007; 56
Belenguer (R38-10-20140418) 2007; 73
Leach (R8-10-20140418) 2008; 28
Jia (R10-10-20140418) 2010; 310
Levine (R30-10-20140418) 1998; 93
Buchanan (R12-10-20140418) 2009; 30
Sokol (R23-10-20140418) 2009; 15
Sokol (R22-10-20140418) 2008; 105
Beattie (R2-10-20140418) 1998; 14
Gerasimidis (R14-10-20140418) 2011; 45
Vetrovsky (R20-10-20140418) 2013; 8
Lewis (R34-10-20140418) 2007; 102
Hansen (R24-10-20140418) 2013; 8
Moore (R32-10-20140418) 1998; 43
Whelan (R39-10-20140418) 2005; 135
Sartor (R5-10-20140418) 2011; 4
Fiorucci (R35-10-20140418) 2006; 131
Lionetti (R7-10-20140418) 2005; 29
Silverberg (R21-10-20140418) 2005; 19
Cameron (R1-10-20140418) 2013; 37
Laurentin (R16-10-20140418) 2004; 43
Fiorucci (R36-10-20140418) 2007; 150
Roediger (R27-10-20140418) 1980; 2
Thibault (R28-10-20140418) 2007; 133
Tjellstrom (R11-10-20140418) 2012; 47
24859301 - Inflamm Bowel Dis. 2014 Jul;20(7):E18. doi: 10.1097/MIB.0000000000000071.
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References_xml – volume: 47
  start-page: 1454
  year: 2012
  ident: R11-10-20140418
  publication-title: Scand J Gastroenterol
  doi: 10.3109/00365521.2012.703234
– volume: 2
  start-page: 712
  year: 1980
  ident: R27-10-20140418
– volume: 15
  start-page: 75
  year: 1992
  ident: R17-10-20140418
  publication-title: J Microbiol Methods
  doi: 10.1016/0167-7012(92)90071-B
– volume: 105
  start-page: 16731
  year: 2008
  ident: R22-10-20140418
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.0804812105
– volume: 18
  start-page: 1672
  year: 2012
  ident: R13-10-20140418
  publication-title: Inflamm Bowel Dis
  doi: 10.1002/ibd.21916
– volume: 14
  start-page: 345
  year: 1998
  ident: R2-10-20140418
  publication-title: Nutrition
  doi: 10.1016/S0899-9007(97)00493-0
– volume: 133
  start-page: 1916
  year: 2007
  ident: R28-10-20140418
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2007.08.041
– volume: 41
  start-page: 77
  year: 1997
  ident: R29-10-20140418
  publication-title: Gut
  doi: 10.1136/gut.41.1.77
– volume: 150
  start-page: 996
  year: 2007
  ident: R36-10-20140418
  publication-title: Br J Pharmacol
  doi: 10.1038/sj.bjp.0707193
– volume: 12
  start-page: 439
  year: 1991
  ident: R15-10-20140418
  publication-title: J Pediatr Gastroenterol Nutr
  doi: 10.1097/00005176-199105000-00005
– volume: 52
  start-page: 237
  year: 2003
  ident: R19-10-20140418
  publication-title: Gut
  doi: 10.1136/gut.52.2.237
– volume: 8
  start-page: e57923
  year: 2013
  ident: R20-10-20140418
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0057923
– volume: 131
  start-page: 259
  year: 2006
  ident: R35-10-20140418
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2006.02.033
– volume: 30
  start-page: 501
  year: 2009
  ident: R12-10-20140418
  publication-title: Aliment Pharmacol Ther
  doi: 10.1111/j.1365-2036.2009.04067.x
– volume: 56
  start-page: 1543
  year: 2007
  ident: R26-10-20140418
  publication-title: Gut
  doi: 10.1136/gut.2006.108449
– volume: 102
  start-page: 624
  year: 2007
  ident: R34-10-20140418
  publication-title: Am J Gastroenterol
  doi: 10.1111/j.1572-0241.2006.01020.x
– volume: 134
  start-page: 577
  year: 2008
  ident: R4-10-20140418
  publication-title: Gastroenterology
  doi: 10.1053/j.gastro.2007.11.059
– volume: 29
  start-page: S173
  year: 2005
  ident: R7-10-20140418
  publication-title: JPEN J Parenter Enteral Nutr
  doi: 10.1177/01486071050290S4S173
– volume: 19
  start-page: 5
  year: 2005
  ident: R21-10-20140418
  publication-title: Can J Gastroenterol
  doi: 10.1155/2005/269076
– volume: 43
  start-page: 183
  year: 2004
  ident: R16-10-20140418
  publication-title: Eur J Nutr
  doi: 10.1007/s00394-004-0457-3
– volume: 93
  start-page: 83
  year: 1998
  ident: R30-10-20140418
  publication-title: Am J Gastroenterol
  doi: 10.1111/j.1572-0241.1998.083_c.x
– volume: 46
  start-page: 1722
  year: 2001
  ident: R31-10-20140418
  publication-title: Dig Dis Sci
  doi: 10.1023/A:1010661706385
– volume: 43
  start-page: 162
  year: 1998
  ident: R32-10-20140418
  publication-title: Dig Dis Sci
  doi: 10.1023/A:1018848709769
– volume: 12
  start-page: 106
  year: 2006
  ident: R18-10-20140418
  publication-title: Inflamm Bowel Dis
  doi: 10.1097/01.MIB.0000200323.38139.c6
– volume: 8
  start-page: e58825
  year: 2013
  ident: R24-10-20140418
  publication-title: PLoS One
  doi: 10.1371/journal.pone.0058825
– volume: 38
  start-page: 870
  year: 1996
  ident: R37-10-20140418
  publication-title: Gut
  doi: 10.1136/gut.38.6.870
– volume: 4
  start-page: 127
  year: 2011
  ident: R5-10-20140418
  publication-title: Mucosal Immunol
  doi: 10.1038/mi.2010.87
– volume: 63
  start-page: 105
  year: 2004
  ident: R6-10-20140418
  publication-title: Proc Nutr Soc
  doi: 10.1079/PNS2003317
– volume: 44
  start-page: 736
  year: 2012
  ident: R9-10-20140418
  publication-title: Dig Liver Dis
  doi: 10.1016/j.dld.2012.04.014
– volume: 73
  start-page: 6526
  year: 2007
  ident: R38-10-20140418
  publication-title: Appl Environ Microbiol
  doi: 10.1128/AEM.00508-07
– volume: 45
  start-page: 234
  year: 2011
  ident: R14-10-20140418
  publication-title: J Clin Gastroenterol
  doi: 10.1097/MCG.0b013e3181f39af5
– volume: 104
  start-page: 693
  year: 2010
  ident: R25-10-20140418
  publication-title: Br J Nutr
  doi: 10.1017/S0007114510001030
– volume: 37
  start-page: 622
  year: 2013
  ident: R1-10-20140418
  publication-title: Aliment Pharmacol Ther
  doi: 10.1111/apt.12230
– volume: 15
  start-page: 1183
  year: 2009
  ident: R23-10-20140418
  publication-title: Inflamm Bowel Dis
  doi: 10.1002/ibd.20903
– volume: 41
  start-page: 70
  year: 1997
  ident: R33-10-20140418
  publication-title: Gut
  doi: 10.1136/gut.41.1.70
– volume: 135
  start-page: 1896
  year: 2005
  ident: R39-10-20140418
  publication-title: J Nutr
  doi: 10.1093/jn/135.8.1896
– volume: 136
  start-page: 285
  year: 2000
  ident: R3-10-20140418
  publication-title: Nutrition as primary therapy in pediatric Crohns disease: fact or fantasy J Pediatr
– volume: 310
  start-page: 138
  year: 2010
  ident: R10-10-20140418
  publication-title: Is the abundance of Faecalibacterium prausnitzii relevant to Crohns disease FEMS Microbiol Lett
– volume: 28
  start-page: 724
  year: 2008
  ident: R8-10-20140418
  publication-title: Aliment Pharmacol Ther
  doi: 10.1111/j.1365-2036.2008.03796.x
– reference: 24859301 - Inflamm Bowel Dis. 2014 Jul;20(7):E18. doi: 10.1097/MIB.0000000000000071.
– reference: 24859302 - Inflamm Bowel Dis. 2014 Jul;20(7):E18-9. doi: 10.1097/MIB.0000000000000079.
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Snippet The gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of...
The gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its mode of...
BackgroundThe gut microbiota is implicated in the pathogenesis of Crohn’s disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its...
Background: The gut microbiota is implicated in the pathogenesis of Crohn's disease (CD). Exclusive enteral nutrition (EEN) is a successful treatment, but its...
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SubjectTerms Adolescent
Bacteria
Bacteroides
Biomarkers - metabolism
Case-Control Studies
Child
Crohn Disease - metabolism
Crohn Disease - microbiology
Crohn Disease - prevention & control
Crohn's disease
Enteral Nutrition
Faecalibacterium prausnitzii
Feces
Feces - chemistry
Feces - microbiology
Female
Follow-Up Studies
Gastrointestinal Tract - metabolism
Gastrointestinal Tract - microbiology
Humans
Male
Metabolites
Metabolomics
Microbiota
Nutrition
Prevotella
Prognosis
Remission Induction
Title Decline in Presumptively Protective Gut Bacterial Species and Metabolites Are Paradoxically Associated with Disease Improvement in Pediatric Crohn’s Disease During Enteral Nutrition
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