PubMed · 9923255
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K F Jeter. 1998. A reminder.. https://pubmed.ncbi.nlm.nih.gov/9923255/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
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.
Among etiological factors suspected of causing Crohn's disease a number of bacteria was listed (Yersinia, Mycobacterium kansasi, Mycobacterium pseudotuberculosis) as well as viruses (measles). None of them however can be considered as the only agent. As to external influences, we know the adverse effect of smoking, the toxic effect Al and oral contraceptives. The listed causes may enhance the development of mesenteric thromboses or immunocomplex vasculitis with ischaemization of a certain portion of the small or large intestine with subsequent inflammation. So far we do not know what starts the immunological reaction, but subsequently the process takes place via cytokines, prostaglandin PGE2, leukotriene LTB4 and liberation of free oxygen radicals (this knowledge is applied in therapy). The authors discuss the problem whether Crohn's disease is one clinical entity with a different course or whether a single diagnosis comprises two or more pathological units.
Explore the source record for details and available documents.