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    Home > Active Ingredient News > Study of Nervous System > Cell Host & Microbe nerve signals regulate surface glycosylation of intestinal epithelial cells and gut microbial homeostasis

    Cell Host & Microbe nerve signals regulate surface glycosylation of intestinal epithelial cells and gut microbial homeostasis

    • Last Update: 2022-10-01
    • Source: Internet
    • Author: User
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    The intestines are inhabited by tens of thousands of microorganisms, which have important effects on the health, metabolism regulation, and immune regulation of
    the host.

    At the same time, the intestine is also the organ in the body with the highest number of neurons besides the brain
    .

    The presence of a large number of sensory neurons (80% of afferent neurons) and motor neurons (20% of efferent neurons) in the gut indicates that communication between the brain and the
    gut is bidirectional.

    Numerous studies have shown that the gut microbiome, and the metabolites from which they originate, can regulate neuronal activity in the brain through different pathways, but whether and how neurons regulate the behavior and homeostasis of the gut microbiome remains unclear
    .



    On September 22, 2022, the Zhongbin Deng team from the University of Louisville published an article in Cell Host & Microbe Enteric VIP-producing neurons maintain gut microbiota homeostasis through regulating epithelium fucosylation.
    It was demonstrated that VIP neurons regulate fucosification modifications on the surface of intestinal epithelial cells by secreting VIP-signaling peptides, thereby regulating the colonization and homeostasis
    of intestinal microorganisms in the intestine.




    The vagus nerve is the main nerve responsible for intestinal-brain communication, and the authors have proved that the vagus nerve can regulate the expression of fut2, the gene responsible for fucosification modification in intestinal epithelial cells, thereby regulating the level
    of fucosification modification on the surface of intestinal epithelial cells.


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    .


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