Gut microbiota dysfunction in Crohn’s disease

IntroductionCrohn’s disease (CD) results from alterations in the gut microbiota and the immune system. However, the exact metabolic dysfunctions of the gut microbiota during CD are still unclear. Here, we investigated metagenomic functions using PICRUSt2 during the course of CD to better understand...

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Main Authors: Sylvie Buffet-Bataillon, Gabriela Durão, Isabelle Le Huërou-Luron, Olivier Rué, Yann Le Cunff, Vincent Cattoir, Guillaume Bouguen
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-02-01
Series:Frontiers in Cellular and Infection Microbiology
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Online Access:https://www.frontiersin.org/articles/10.3389/fcimb.2025.1540352/full
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author Sylvie Buffet-Bataillon
Sylvie Buffet-Bataillon
Gabriela Durão
Isabelle Le Huërou-Luron
Olivier Rué
Olivier Rué
Yann Le Cunff
Vincent Cattoir
Guillaume Bouguen
author_facet Sylvie Buffet-Bataillon
Sylvie Buffet-Bataillon
Gabriela Durão
Isabelle Le Huërou-Luron
Olivier Rué
Olivier Rué
Yann Le Cunff
Vincent Cattoir
Guillaume Bouguen
author_sort Sylvie Buffet-Bataillon
collection DOAJ
description IntroductionCrohn’s disease (CD) results from alterations in the gut microbiota and the immune system. However, the exact metabolic dysfunctions of the gut microbiota during CD are still unclear. Here, we investigated metagenomic functions using PICRUSt2 during the course of CD to better understand microbiota-related disease mechanisms and provide new insights for novel therapeutic strategies.MethodsWe performed 16S rRNA-based microbial profiling of 567 faecal samples collected from a cohort of 383 CD patients, including 291 remissions (CR), 177 mild-moderate (CM) and 99 severe (CS) disease states. Gene and pathway composition was assessed using PICRUSt2 analyses of 16S data.ResultsAs expected, changes in alpha and beta diversity, in interaction networks and increases in Proteobacteria abundance were associated with disease severity. However, microbial function was more consistently disrupted than composition from CR, to CM and then to CS. Major shifts in oxidative stress pathways and reduced carbohydrate and amino acid metabolism in favour of nutrient transport were identified in CS compared to CR. Virulence factors involved in host invasion, host evasion and inflammation were also increased in CS.ConclusionsThis functional metagenomic information provides new insights into community-wide microbial processes and pathways associated with CD pathogenesis. This study paves the way for new advanced strategies to rebalance gut microbiota and/or eliminate oxidative stress, and biofilm to downregulate gut inflammation.
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spelling doaj-art-8784ee1e84c14dd5a4a0b555e8c3f2242025-02-11T06:59:58ZengFrontiers Media S.A.Frontiers in Cellular and Infection Microbiology2235-29882025-02-011510.3389/fcimb.2025.15403521540352Gut microbiota dysfunction in Crohn’s diseaseSylvie Buffet-Bataillon0Sylvie Buffet-Bataillon1Gabriela Durão2Isabelle Le Huërou-Luron3Olivier Rué4Olivier Rué5Yann Le Cunff6Vincent Cattoir7Guillaume Bouguen8Department of Clinical Microbiology, CHU Rennes, Rennes, FranceInstitut NUMECAN, INRAE, INSERM, Univ Rennes, Rennes, FranceDepartment of Clinical Microbiology, CHU Rennes, Rennes, FranceInstitut NUMECAN, INRAE, INSERM, Univ Rennes, Rennes, FranceUniversité Paris-Saclay, INRAE, MaIAGE, Jouy-en-Josas, FranceUniversité Paris-Saclay, INRAE, BioinfOmics, MIGALE Bioinformatics Facility, Jouy-en-Josas, FranceIRISA, Univ Rennes, Inria, CNRS, Rennes, FranceDepartment of Clinical Microbiology, CHU Rennes, Rennes, FranceCHU Rennes, Univ Rennes, INSERM, U1230, Rennes, FranceIntroductionCrohn’s disease (CD) results from alterations in the gut microbiota and the immune system. However, the exact metabolic dysfunctions of the gut microbiota during CD are still unclear. Here, we investigated metagenomic functions using PICRUSt2 during the course of CD to better understand microbiota-related disease mechanisms and provide new insights for novel therapeutic strategies.MethodsWe performed 16S rRNA-based microbial profiling of 567 faecal samples collected from a cohort of 383 CD patients, including 291 remissions (CR), 177 mild-moderate (CM) and 99 severe (CS) disease states. Gene and pathway composition was assessed using PICRUSt2 analyses of 16S data.ResultsAs expected, changes in alpha and beta diversity, in interaction networks and increases in Proteobacteria abundance were associated with disease severity. However, microbial function was more consistently disrupted than composition from CR, to CM and then to CS. Major shifts in oxidative stress pathways and reduced carbohydrate and amino acid metabolism in favour of nutrient transport were identified in CS compared to CR. Virulence factors involved in host invasion, host evasion and inflammation were also increased in CS.ConclusionsThis functional metagenomic information provides new insights into community-wide microbial processes and pathways associated with CD pathogenesis. This study paves the way for new advanced strategies to rebalance gut microbiota and/or eliminate oxidative stress, and biofilm to downregulate gut inflammation.https://www.frontiersin.org/articles/10.3389/fcimb.2025.1540352/fullCrohn’s diseasemicrobiotametabolic functionstreatmentoxidative stress
spellingShingle Sylvie Buffet-Bataillon
Sylvie Buffet-Bataillon
Gabriela Durão
Isabelle Le Huërou-Luron
Olivier Rué
Olivier Rué
Yann Le Cunff
Vincent Cattoir
Guillaume Bouguen
Gut microbiota dysfunction in Crohn’s disease
Frontiers in Cellular and Infection Microbiology
Crohn’s disease
microbiota
metabolic functions
treatment
oxidative stress
title Gut microbiota dysfunction in Crohn’s disease
title_full Gut microbiota dysfunction in Crohn’s disease
title_fullStr Gut microbiota dysfunction in Crohn’s disease
title_full_unstemmed Gut microbiota dysfunction in Crohn’s disease
title_short Gut microbiota dysfunction in Crohn’s disease
title_sort gut microbiota dysfunction in crohn s disease
topic Crohn’s disease
microbiota
metabolic functions
treatment
oxidative stress
url https://www.frontiersin.org/articles/10.3389/fcimb.2025.1540352/full
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