The intestinal microbiota is known to influence postnatal growth. We previously found that a strain of
Lactiplantibacillus plantarum
(strain Lp
WJL
) buffers the adverse effects of chronic undernutrition on the growth of juvenile germ-free mice. Here, we report that Lp
WJL
sustains the postnatal growth of malnourished conventional animals and supports both insulin-like growth factor–1 (IGF-1) and insulin production and activity. We have identified cell walls isolated from Lp
WJL
, as well as muramyl dipeptide and mifamurtide, as sufficient cues to stimulate animal growth despite undernutrition. Further, we found that NOD2 is necessary in intestinal epithelial cells for Lp
WJL
-mediated IGF-1 production and for postnatal growth promotion in malnourished conventional animals. These findings indicate that, coupled with renutrition, bacteria cell walls or purified NOD2 ligands have the potential to alleviate stunting.
The gastrointestinal tract harbors an intrinsic neuronal network, the enteric nervous system (ENS). The ENS controls motility, fluid homeostasis and blood flow, but also interacts with other components of the intestine such as epithelial and immune cells. Recent studies indicate that gut microbiota diversification occurring concomitantly to postnatal ENS maturation could be critical for ENS development and function. Here we discuss the possibility that this functional relationship starts in utero, whereby the maternal microbiota would prime the developing ENS and shape its physiology. We review the ENS/microbiota interactions and their modulation in physiological and pathophysiological contexts. While the microbial modulation of ENS physiology is now well established, further studies are required to understand the contribution of the gut microbiota to the ENS development and pathologies and to reveal the precise mechanisms underlying microbiota-to-ENS communications.
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