Gut microbiota and IBD

doi:10.1016/S0399-8320(10)70020-8

Gastroentérologie Clinique et Biologique

Volume 34, Supplement 1, September 2010, Pages S44-S51

https://doi.org/10.1016/S0399-8320(10)70020-8 Get rights and content

Summary

Gut microbiota contains about 10¹⁴ bacterial cells classified within 4 bacterial phyla, namely Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria. Much of the information has been generated through the application of nucleic acid-based methodologies (16S rRNA) which provide a cornerstone of microbial taxonomy. Inflammatory bowel disease (IBD) involves a dysregulated immune response to the gut microbiota in genetically predisposed hosts. Experimental animal models of colitis provide the best evidence that bacteria present in the bowel of the animals have an essential role in the pathogenesis of colitis since in most models, germ-free animals do not develop disease. Moreover, in the immunodeficient mouse model of colitis called TRUC (T-bet-/- x RAG2-/-), a colitogenic gut microbiota is selected and can be transmitted to mice with intact immunity and induce colitis. Current interest therefore focuses on the bacterial community as the source of antigens that fuel the chronic inflammation seen in IBD. Dysbiosis, an imbalance between harmful and protective bacteria, has been evoked and investigated in IBD. Thus, besides the classical pathogens, gut microbiota can drive pathogenicity via two mechanisms: an expansion of ‘pro-inflammatory'species or a restriction in the protective compounds of the microbiota. Complexity of the microbiota suggests that both mechanisms may contribute to chronic gut inflammation in IBD.

Résumé

Le microbiote intestinal contient environ 10¹⁴ bactéries classées en 4 phyla bactériens: Firmicutes, Bacteroidetes, Actinobacteria, et Proteobacteria. Une grande partie des informations concernant cet écosystème a été générée par l’application de méthodes moléculaires visant la reconnaisance des acides nucléiques (16S ARNr) motifs moléculaires clefs de la taxonomie microbienne. Les maladies inflammatoires de l’intestin (MICI) résultent d’une réponse immunitaire dérégulée vis-à-vis du microbiote intestinal chez des sujets génétiquement prédisposés. Les modèles murins de colite expérimentale fournissent des arguments expérimentaux solides pour incriminer la microflore intestinale dans la pathogenèse d’une colite. En effet, dans la plupart des modèles, la colite ne se développe pas en absence de microbiote (situation axénique). Récemment, avec le modèle de souris immunodéficientes de colite appelée TRUC (T-bet^{– /–} x RAG2^{– /–} , ulcerative colitis), un nouveau paradigme a emergé puisque le microbiote intestinal semble pouvoir transmettre la colite suggérant ainsi l’existence d’un microbiote ‘colitogénique’. Un intérêt grandissant centré sur l’étude des communautés bactériennes comme source antigénique alimentant l’inflammation chronique au cours des MICI a vu le jour. Une dysbiose, i.e. un déséquilibre entre des bactéries ‘délétères’et ‘bénéfiques’, a été évoquée et recherchée dans les MICI. A côté des agents pathogènes classiques, le microbiote intestinal pourrait porter une pathogénicité de deux façons: par l’expansion d’espèces «proinflammatoires» ou par la diminution de bactéries protectrices « anti-inflammatoires ». La complexité du microbiote suggère que ces deux mécanismes pourraient contribuer à l’inflammation intestinale chronique rencontrée au cours des MICI.

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Le microbiote intestinal humain est composé de 10¹⁴ bactéries ainsi que d’autres micro-organismes comme les virus, les champignons et les archées. L’étude du microbiote intestinal a dévoilé le rôle fondamental qu’il joue dans la physiologie intestinale mais aussi dans la santé humaine de façon plus générale, comme un véritable« organe caché ». Dans cette revue, nous exposons la structure et le rôle du microbiote intestinal ainsi que son implication en pathologie humaine. Après la colonisation bactérienne du tube digestif chez le nourrisson, la composition du microbiote intestinal est unique à chaque individu bien que plus de 95 % des bactéries le composant puissent être réparties en 4 phyla majeurs. Des approches culture-indépendantes et, plus récemment, l’avènement du séquençage haut débit ont permis de décrire précisément la structure et la diversité du microbiote intestinal ainsi que son altération en pathologie. Le microbiote intestinal est impliqué dans la maturation du système immunitaire et dans de nombreuses voies métaboliques fondamentales comme la fermentation des sucres et des protéines ainsi que le métabolisme des acides biliaires et des xénobiotiques. Le déséquilibre des populations du microbiote intestinal ou dysbiose a des conséquences fonctionnelles importantes et est impliqué dans de nombreuses pathologies digestives (maladies inflammatoires chroniques intestinales, cancer colorectal, etc.) mais aussi dans l’obésité et l’autisme. Ces observations ont conduit à l’émergence de nombreuses études sur les traitements visant à restaurer l’équilibre du microbiote intestinal comme les probiotiques ou la transplantation du microbiote fécal. Mais des travaux récents sur l’activité de métabolites issus du microbiote pourraient conduire à des perspectives thérapeutiques prometteuses.
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L’utilisation des probiotiques a montré globalement son innocuité, même si quelques risques infectieux chez des personnes sensibles ont parfois été observées. Le champ d’utilisation des probiotiques est de plus en plus vaste. Les pathologies les couramment ciblées sont les diarrhées, maladies inflammatoires chroniques intestinales et allergies. D’autres pathologies commencent à s’intéresser à l’approche probiotique comme l’obésité, les maladies métaboliques, ainsi que les maladies psychiatriques. D’autres utilisations moins courantes sont évoquées. Les effets observés sont variables selon les souches utilisées et les populations ciblées rendant dans de nombreuses indications leur recommandation par les comités d’experts difficile aujourd’hui. Cependant, les effets bénéfiques observés dans certaines études sont encourageants, justifiant la poursuite des études expérimentales afin d’améliorer la sélection de souches efficaces et d’essais cliniques contrôlés comportant un nombre suffisant de patients.
La modulation du microbiote intestinal par les probiotiques est une approche extrêmement séduisante et prometteuse, plutôt dans une approche préventive dans le champ en pleine expansion des pathologies reliées à une dysbiose du microbiote intestinal.
The human gut is a huge complex ecosystem where microbiota, nutrients, and host cells interact extensively, displaying a real partnership with the host. Dysbiosis in the gut microbiota is therefore involved in many diseases.
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Gut microbiota modulation through probiotic administration is an appealing and promising approach of prevention of the numerous diseases linked to gut microbiota impairment.

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^☆: A reprint of the french translation of this article is available on request.

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Gut microbiota and IBDMicrobiote intestinal et MICI☆

Summary

Résumé

Gastroenterology

Gastroenterology

Gastroenterology

Cell

Gastroenterology

Gastroenterology

Clin Microbiol Infect

Am J Gastroenterol

Lancet

Gastroenterology

FEMS Microbiol Ecol

Role of the faecal stream in the maintenance of Crohn's colitis

Gut

Mucosal colonisation with Lactobacillus casei mitigates barrier injury induced by exposure to trinitronbenzene sulphonic acid

Gut

Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease

Nature

Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract

Science

Differential effects of NOD2 variants on Crohn's disease risk and phenotype in diverse populations: a metaanalysis

Am J Gastroenterol

A genome-wide association study identifies IL23R as an inflammatory bowel disease gene

Science

Genome-wide association study identifies new susceptibility loci for Crohn disease and implicates autophagy in disease pathogenesis

Nat Genet

NOD2 (CARD15) mutations in Crohn‘s disease are associated with diminished mucosal {alpha}-defensin expression

Gut

Inducible and constitutive beta-defensins are differentially expressed in Crohn‘s disease and ulcerative colitis

Inflamm Bowel Dis

Reduced alpha-defensin expression is associated with inflammation and not NOD2 mutation status in ileal Crohn‘s disease

Gut

Mucosal antibodies in inflammatory bowel disease are directed against intestinal bacteria

Gut

Colonic bacteria express an ulcerative colitis pANCA-related protein epitope

Infect Immun