Bifidobacteria-mediated immune system imprinting early in life
By B. Henrick, L. Rodriguez, T. Lakshmikanth, Christian Pou, E. Henckel, Axel Olin, Jun Wang, J. Mikeš, Ziyang Tan, Yang Chen and 16 more. bioRxiv, 2020
674 citations recorded by the source corpus.
Immune-microbe interactions early in life influence an individual’s risk of developing allergies, asthma and some autoimmune disorders. Breastfeeding helps guide the development of healthy immune-microbe relationships, in part by providing nutrients to specialized microbes that in turn benefit the host and its developing immune system. Such bacteria having co-evolved with humans are associated with reduced risks of immune mediated diseases but are increasingly rare in modern societies. Here we map an immunological sequence of events, triggered by microbial colonization that distinguish children with different gut bacterial composition. Lack of bifidobacterial species is associated with elevated markers of intestinal inflammation and immune dysregulation and in a randomized trial of breastfed infants, the infant-adapted Bifidobacterium infantis EVC001 silenced intestinal Th2 and Th17 immune responses, while inducing IFNβ, and its metabolites skew T-cell polarization in vitro, from Th2 towards Th1, suggesting a healthier immune imprinting during the first critical months of life. HIGHLIGHTS An ordered sequence of immune changes after birth, driven by microbial interactions Low gut Bifidobacterium abundance is associated with markers of intestinal inflammation Feeding B. infantis EVC001 silenced intestinal Th2 and Th17 but upregulates IFNβ B. infantis EVC001 metabolites and/or enteric cytokines skew naïve T-cell polarization towards Th1 and away from Th2
View Paper: https://www.semanticscholar.org/paper/20d6e8ba9c86d4a85a536d0095d5db568ba62757
Citations in the corpus
- Short-chain fatty acids: linking diet, the microbiome and immunity (2024, unknown): “Targeting Bifidobacteria might be a therapeutic option in this case, as they have evolved in the intestinal niche to express genes for utilization of human milk oligosaccharides from breastmilk, to generate SCFAs and thereby prevent systemic inflammation and immune dysregulation 176 .”