Microbial Modulation of the Development and Physiology of the Enteric Nervous System

The gastrointestinal tract harbors its own intrinsic nervous system, the enteric nervous system (ENS). Nutrients, such as glucose, fatty acids, or amino acids, indirectly modulate the physiology of the ENS. Moreover, recent studies have shown that the gut microbiota is a key regulator of ENS physiology and development. Although most of the development of the ENS occurs in utero, that is, in an environment devoid of microbiota, the maternal microbiota could influence the offspring’s ENS development through bacterial metabolites and microbiota-regulated signaling pathways. During early life, alterations in the gut microbiota, caused for example by antibiotic use, cause long-term changes in the physiology of the ENS. Enteroendocrine and immune cells of the gut are key players in the communication between the microbiota and the ENS. 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. 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.