scholarly journals The Interplay between Nutrition, Innate Immunity, and the Commensal Microbiota in Adaptive Intestinal Morphogenesis

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2198
Author(s):  
Franziska Bayer ◽  
Olga Dremova ◽  
My Phung Khuu ◽  
Könül Mammadova ◽  
Giulia Pontarollo ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Nervous System ◽  
Gut Microbiota ◽  
Enteric Nervous System ◽  
Gut Development ◽  
Embryonic Mouse ◽  
Capillary Networks ◽  
Commensal Microbiota ◽  
Tissue Organization ◽  
Adult Organism

The gastrointestinal tract is a functionally and anatomically segmented organ that is colonized by microbial communities from birth. While the genetics of mouse gut development is increasingly understood, how nutritional factors and the commensal gut microbiota act in concert to shape tissue organization and morphology of this rapidly renewing organ remains enigmatic. Here, we provide an overview of embryonic mouse gut development, with a focus on the intestinal vasculature and the enteric nervous system. We review how nutrition and the gut microbiota affect the adaptation of cellular and morphologic properties of the intestine, and how these processes are interconnected with innate immunity. Furthermore, we discuss how nutritional and microbial factors impact the renewal and differentiation of the epithelial lineage, influence the adaptation of capillary networks organized in villus structures, and shape the enteric nervous system and the intestinal smooth muscle layers. Intriguingly, the anatomy of the gut shows remarkable flexibility to nutritional and microbial challenges in the adult organism.

scholarly journals “Too much guts and not enough brains”: (epi)genetic mechanisms and future therapies of Hirschsprung disease — a review

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Emilie G. Jaroy ◽  
Lourdes Acosta-Jimenez ◽  
Ryo Hotta ◽  
Allan M. Goldstein ◽  
Ragnhild Emblem ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nervous System ◽  
Enteric Nervous System ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Current Knowledge ◽  
Hirschsprung Disease ◽  
Gut Development ◽  
Dna And Rna ◽  
Expression Of Genes

Abstract Hirschsprung disease is a neurocristopathy, characterized by aganglionosis in the distal bowel. It is caused by failure of the enteric nervous system progenitors to migrate, proliferate, and differentiate in the gut. Development of an enteric nervous system is a tightly regulated process. Both the neural crest cells and the surrounding environment are regulated by different genes, signaling pathways, and morphogens. For this process to be successful, the timing of gene expression is crucial. Hence, alterations in expression of genes specific for the enteric nervous system may contribute to the pathogenesis of Hirschsprung’s disease. Several epigenetic mechanisms contribute to regulate gene expression, such as modifications of DNA and RNA, histone modifications, and microRNAs. Here, we review the current knowledge of epigenetic and epitranscriptomic regulation in the development of the enteric nervous system and its potential significance for the pathogenesis of Hirschsprung’s disease. We also discuss possible future therapies and how targeting epigenetic and epitranscriptomic mechanisms may open new avenues for novel treatment.

scholarly journals Influence of Commensal Microbiota on the Enteric Nervous System and Its Role in Neurodegenerative Diseases

2018 ◽  
Vol 10 (3) ◽  
pp. 172-180 ◽  
Author(s):  
Kristina Endres ◽  
Karl-Herbert Schäfer
Keyword(s):  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Enteric Nervous System ◽  
The Other ◽  
Therapeutic Approaches ◽  
Commensal Microbiota ◽  
Open Questions ◽  
Learning Capabilities ◽  
The Central Nervous System ◽  
Parkinson Diseases

When thinking about neurodegenerative diseases, the first symptoms that come to mind are loss of memory and learning capabilities, which all resemble hallmarks of manifestation of such diseases in the central nervous system (CNS). However, the gut comprises the largest nervous system outside the CNS that is autonomously active and in close interplay with its microbiota. Therefore, the enteric nervous system (ENS) might serve as an indicator of degenerative pathomechanisms that also affect the CNS. On the other hand, it might offer an entry point for devastating influences from the microbial community or – conversely – for therapeutic approaches via gut commensals. Within the last years, the ENS and gut microbiota therefore have sparked the interest of researchers of CNS diseases and we here report on recent findings and open questions, especially with regard to Alzheimer and Parkinson diseases.

scholarly journals Host Gut Motility and Bacterial Competition Drive Instability in a Model Intestinal Microbiota

2016 ◽  
Author(s):  
Travis J. Wiles ◽  
Matthew L. Jemielita ◽  
Ryan P. Baker ◽  
Brandon H. Schlomann ◽  
Savannah L. Logan ◽  
...  
Keyword(s):  
Nervous System ◽  
Gut Microbiota ◽  
Enteric Nervous System ◽  
Bacterial Species ◽  
Stochastic Perturbation ◽  
Hirschsprung Disease ◽  
Light Sheet ◽  
Mitigation Strategies ◽  
Gut Motility ◽  
Bacterial Competition

AbstractThe gut microbiota is a complex consortium of microorganisms with the ability to influence important aspects of host health and development. Harnessing this ‘microbial organ’ for biomedical applications requires clarifying the degree to which host and bacterial factors act alone or in combination to govern the stability of specific lineages. To address this we combined bacteriological manipulation and light sheet fluorescence microscopy to monitor the dynamics of a defined two-species microbiota within the vertebrate gut. We observed that the interplay between each population and the gut environment produced distinct spatiotemporal patterns. Consequently, one species dominates while the other experiences dramatic collapses that are well fit by a stochastic mathematical model. Modeling revealed that bacterial competition could only partially explain the observed phenomena, suggesting that a host factor is also important in shaping the community. We hypothesized the host determinant to be gut motility, and tested this mechanism by measuring colonization in hosts with enteric nervous system dysfunction due to mutation in the Hirschsprung disease locus ret. In mutant hosts we found reduced gut motility and, confirming our hypothesis, robust coexistence of both bacterial species. This study provides evidence that host-mediated spatial structuring and stochastic perturbation of communities along with bacterial competition drives population dynamics within the gut. In addition, this work highlights the capacity of the enteric nervous system to affect stability of gut microbiota constituents, demonstrating that the ‘gut-brain axis’ is bidirectional. Ultimately, these findings will help inform disease mitigation strategies focused on engineering the intestinal ecosystem.

scholarly journals Fecal Supernatant from Adult with Autism Spectrum Disorder Alters Digestive Functions, Intestinal Epithelial Barrier, and Enteric Nervous System

2021 ◽  
Vol 9 (8) ◽  
pp. 1723
Author(s):  
Jacques Gonzales ◽  
Justine Marchix ◽  
Laetitia Aymeric ◽  
Catherine Le Berre-Scoul ◽  
Johanna Zoppi ◽  
...  
Keyword(s):  
Nervous System ◽  
Gut Microbiota ◽  
Enteric Nervous System ◽  
Fecal Microbiota ◽  
Autism Spectrum ◽  
Repetitive Behaviors ◽  
Rrna Gene ◽  
Intestinal Epithelial ◽  
Microbiota Composition ◽  
Α Diversity

Autism Spectrum Disorders (ASDs) are neurodevelopmental disorders defined by impaired social interactions and communication with repetitive behaviors, activities, or interests. Gastrointestinal (GI) disturbances and gut microbiota dysbiosis are frequently associated with ASD in childhood. However, it is not known whether microbiota dysbiosis in ASD patients also occurs in adulthood. Further, the consequences of altered gut microbiota on digestive functions and the enteric nervous system (ENS) remain unexplored. Therefore, we studied, in mice, the ability offecal supernatant (FS) from adult ASD patients to induce GI dysfunctions and ENS remodeling. First, the analyses of the fecal microbiota composition in adult ASD patients indicated a reduced α-diversity and increased abundance of three bacterial 16S rRNA gene amplicon sequence variants compared to healthy controls (HC). The transfer of FS from ASD patients (FS–ASD) to mice decreased colonic barrier permeability by 29% and 58% compared to FS–HC for paracellular and transcellular permeability, respectively. These effects are associated with the reduced expression of the tight junction proteins JAM-A, ZO-2, cingulin, and proinflammatory cytokines TNFα and IL1β. In addition, the expression of glial and neuronal molecules was reduced by FS–ASD as compared to FS-HC in particular for those involved in neuronal connectivity (βIII-tubulin and synapsin decreased by 31% and 67%, respectively). Our data suggest that changes in microbiota composition in ASD may contribute to GI alterations, and in part, via ENS remodeling.

scholarly journals Building a brain in the gut: development of the enteric nervous system

2013 ◽  
Vol 83 (4) ◽  
pp. 307-316 ◽  
Author(s):  
AM Goldstein ◽  
RMW Hofstra ◽  
AJ Burns
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Gut Development

scholarly journals Gut Susceptibility to Viral Invasion: Contributing Roles of Diet, Microbiota and Enteric Nervous System to Mucosal Barrier Preservation

2021 ◽  
Vol 22 (9) ◽  
pp. 4734
Author(s):  
Marcela Julio-Pieper ◽  
Alejandra López-Aguilera ◽  
Johana Eyzaguirre-Velásquez ◽  
Loreto Olavarría-Ramírez ◽  
Claudia Ibacache-Quiroga ◽  
...  
Keyword(s):  
Nervous System ◽  
Gut Microbiota ◽  
Enteric Nervous System ◽  
Rich Source ◽  
Mucosal Barrier ◽  
Systemic Complications ◽  
Tissue Invasion ◽  
Pathogenic Viruses

The gastrointestinal lumen is a rich source of eukaryotic and prokaryotic viruses which, together with bacteria, fungi and other microorganisms comprise the gut microbiota. Pathogenic viruses inhabiting this niche have the potential to induce local as well as systemic complications; among them, the viral ability to disrupt the mucosal barrier is one mechanism associated with the promotion of diarrhea and tissue invasion. This review gathers recent evidence showing the contributing effects of diet, gut microbiota and the enteric nervous system to either support or impair the mucosal barrier in the context of viral attack.

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