PubMed · 7380216
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G C Sturniolo, G Mastropaolo, R Naccarato. 1980. Zinc concentrations.. https://pubmed.ncbi.nlm.nih.gov/7380216/
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Exclusive enteral nutrition (EEN) is a first-line therapy for pediatric Crohn's disease (CD), but protective mechanisms remain unknown. We established a prospective pediatric cohort to characterize the function of fecal microbiota and metabolite changes of treatment-naive CD patients in response to EEN (German Clinical Trials DRKS00013306). Integrated multi-omics analysis identified network clusters from individually variable microbiome profiles, with Lachnospiraceae and medium-chain fatty acids as protective features. Bioorthogonal non-canonical amino acid tagging selectively identified bacterial species in response to medium-chain fatty acids. Metagenomic analysis identified high strain-level dynamics in response to EEN. Functional changes in diet-exposed fecal microbiota were further validated using gut chemostat cultures and microbiota transfer into germ-free Il10-deficient mice. Dietary model conditions induced individual patient-specific strain signatures to prevent or cause inflammatory bowel disease (IBD)-like inflammation in gnotobiotic mice. Hence, we provide evidence that EEN therapy operates through explicit functional changes of temporally and individually variable microbiome profiles.
The chronic inflammation in Crohn's disease may be caused by aggressive response to bacterial antigens normal to the gut. Genetic and environmental factors modify the inflammatory response evoked by damage to the mucosal gut barrier. Genetic factors may also determine the subsequent course of chronic inflammation. Further elucidation of the pathogenesis might improve our understanding of the heterogenous nature of Crohn's disease, thus enabling the disease to be subtyped and individualised therapy directed primarily at down-regulation of helper T-cell-1 response to be developed.
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