ABSTRACT
The gut microbiota has the capacity to metabolize food-derived molecules. In this issue of Cell Host & Microbe, Li et al. explore how some bacterial species of the gut microbiota can deplete amino acids in the gut lumen, modulating the amino acid landscape and energy metabolism of the host.
Subject(s)
Amino Acids , Energy Metabolism , Gastrointestinal Microbiome , Gastrointestinal Microbiome/physiology , Amino Acids/metabolism , Humans , Bacteria/metabolism , Bacteria/genetics , Animals , Host Microbial Interactions , Gastrointestinal Tract/microbiologyABSTRACT
The intestinal microbiota is known to influence postnatal growth. We previously found that a strain of Lactiplantibacillus plantarum (strain LpWJL) buffers the adverse effects of chronic undernutrition on the growth of juvenile germ-free mice. Here, we report that LpWJL 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 LpWJL, 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 LpWJL-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.
Subject(s)
Gastrointestinal Microbiome , Growth , Intestines , Lactobacillaceae , Malnutrition , Nod2 Signaling Adaptor Protein , Animals , Mice , Cell Wall/chemistry , Epithelial Cells/microbiology , Epithelial Cells/physiology , Gastrointestinal Microbiome/physiology , Germ-Free Life , Growth Disorders/physiopathology , Growth Disorders/therapy , Insulin/metabolism , Insulin-Like Growth Factor I/metabolism , Intestinal Mucosa/microbiology , Intestinal Mucosa/physiology , Intestines/microbiology , Intestines/physiology , Lactobacillaceae/physiology , Malnutrition/physiopathology , Malnutrition/therapy , Nod2 Signaling Adaptor Protein/metabolism , Growth/drug effects , Growth/physiology , Acetylmuramyl-Alanyl-Isoglutamine/pharmacology , Acetylmuramyl-Alanyl-Isoglutamine/therapeutic useABSTRACT
The worrying number of children suffering from undernutrition and consequent stunting worldwide makes the understanding of the relationship between nutritional status and postnatal growth crucial. Moreover, it is now well established that undernourished children harbor an altered microbiota, correlating with impaired growth. In this review, we describe how murine models have been used to explore the functional relationships between endocrine regulation of growth, nutrition and gut microbiota. In numerous Mammalian species, postnatal growth is mainly regulated by the conserved GH/IGF1 somatotropic axis that acts through endocrine and paracrine pathways, notably enabling longitudinal bone growth. Recent studies have demonstrated that the microbiota effects on growth could involve a modulation of GH and IGF1 circulating levels. Besides, the GH/IGF1 somatotropic axis may regulate the gut microbiota composition and diversity. Studying the bidirectional relationship between growth hormones and the gut microbiome could therefore help developing microbiota-targeting therapies in order to reduce the long-term consequences of stunting.
Subject(s)
Endocrine System/microbiology , Growth and Development , Nutritional Status , Animals , Gastrointestinal Microbiome , Growth Hormone/metabolism , Humans , Insulin-Like Growth Factor I/metabolismABSTRACT
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, which occurs alongside postnatal ENS maturation, could be critical for the development and function of the ENS. 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 ENS/microbiota interactions and their modulation in physiological and pathophysiological contexts. While microbial modulation of the ENS physiology is now well established, further studies are required to understand the contribution of the gut microbiota to the development and pathology of the ENS and to reveal the precise mechanisms underlying microbiota-to-ENS communications.
