Infant Microbiota Communities and Human Milk Oligosaccharide Supplementation Independently and Synergistically Shape Metabolite Production and Immune Responses in Healthy Mice
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Le résumé fourni par la source
BACKGROUND: Multiple studies have demonstrated associations between the early-life gut microbiome and incidence of inflammatory and autoimmune disease in childhood. Although microbial colonization is necessary for proper immune education, it is not well understood at a mechanistic level how specific communities of bacteria promote immune maturation or drive immune dysfunction in infancy. OBJECTIVES: In this study, we aimed to assess whether infant microbial communities with different overall structures differentially influence immune and gastrointestinal development in healthy mice. METHODS: Germ-free mice were inoculated with fecal slurries from Bifidobacterium longum subspecies infantis positive (BIP) or B. longum subspecies infantis negative (BIN) breastfed infants; half of the mice in each group were also supplemented with a pool of human milk oligosaccharides (HMOs) for 14 d. Cecal microbiome composition and metabolite production, systemic and mucosal immune outcomes, and intestinal morphology were assessed at the end of the study. RESULTS: The results showed that inoculation with a BIP microbiome results in a remarkably distinct microbial community characterized by higher relative abundances of cecal Clostridium senu stricto, Ruminococcus gnavus, Cellulosilyticum sp., and Erysipelatoclostridium sp. The BIP microbiome produced 2-fold higher concentrations of cecal butyrate, promoted branched short-chain fatty acid (SCFA) production, and further modulated serotonin, kynurenine, and indole metabolism relative to BIN mice. Further, the BIP microbiome increased the proportions of innate and adaptive immune cells in spleen, while HMO supplementation increased proliferation of mesenteric lymph node cells to phorbol myristate acetate and lipopolysaccharide and increased serum IgA and IgG concentrations. CONCLUSIONS: Different microbiome compositions and HMO supplementation can modulate SCFA and tryptophan metabolism and innate and adaptive immunity in young, healthy mice, with potentially important implications for early childhood health.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Infant Microbiota Communities and Human Milk Oligosaccharide Supplementation Independently and Synergistically Shape Metabolite Production and Immune Responses in Healthy Mice
- Date Crossref
- 01/09/2024
- Éditeur
- Elsevier BV
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Arkansas Children's Nutrition Center pays non établi dans la noticeOrganisme public
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Golisano Children's Hospital pays non établi dans la noticeÉtablissement de santé
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University of Rochester Department of Pediatrics pays non établi dans la noticeUniversité ou école supérieure
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Texas Tech University pays non établi dans la noticeUniversité ou école supérieure
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University of California San Diego Larsson-Rosenquist Foundation Mother-Milk-Infant Center of Research Excellence pays non établi dans la noticeUniversité ou école supérieure
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Virginia Tech pays non établi dans la noticeUniversité ou école supérieure
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University of Arkansas for Medical Sciences pays non établi dans la noticeUniversité ou école supérieure
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University of Rochester Medicine pays non établi dans la noticeÉtablissement de santé
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Microbiome and Metabolism Research Unit SEA pays non établi dans la noticeStructure de recherche
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School of Veterinary Medicine pays non établi dans la noticeUniversité ou école supérieure
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Department of Biomedical Sciences & Pathobiology pays non établi dans la noticeInstitution
Arkansas Children's Nutrition Center, Golisano Children's Hospital et Department of Pediatrics — University of Rochester, avec 8 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.