scholarly journals Emerging roles of gut microbiota and the immune system in the development of the enteric nervous system

2015 ◽  
Vol 125 (3) ◽  
pp. 956-964 ◽  
Author(s):  
Panagiotis S. Kabouridis ◽  
Vassilis Pachnis
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Gut Microbiota ◽  
Enteric Nervous System

scholarly journals Healthy Intestinal Function Relies on Coordinated Enteric Nervous System, Immune System, and Epithelium Responses

Gut Microbes ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 1-14
Author(s):  
Fatima B. Saldana-Morales ◽  
Dasom V. Kim ◽  
Ming-Ting Tsai ◽  
Gretchen E. Diehl
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Enteric Nervous System ◽  
Intestinal Function

scholarly journals Immune system control of rat and rabbit colonic electrolyte transport. Role of prostaglandins and enteric nervous system.

1989 ◽  
Vol 83 (6) ◽  
pp. 1810-1820 ◽  
Author(s):  
M J Bern ◽  
C W Sturbaum ◽  
S S Karayalcin ◽  
H M Berschneider ◽  
J T Wachsman ◽  
...  
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Enteric Nervous System ◽  
Electrolyte Transport ◽  
System Control

scholarly journals Emerging neuropeptide targets in inflammation: NPY and VIP

2013 ◽  
Vol 304 (11) ◽  
pp. G949-G957 ◽  
Author(s):  
Bindu Chandrasekharan ◽  
Behtash Ghazi Nezami ◽  
Shanthi Srinivasan
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Enteric Nervous System ◽  
Intracellular Signaling ◽  
Enteric Neurons ◽  
Vast Number ◽  
Paracrine Effects ◽  
Intracellular Signaling Pathways ◽  
Inflammatory Processes ◽  
Epithelial Secretion

The enteric nervous system (ENS), referred to as the “second brain,” comprises a vast number of neurons that form an elegant network throughout the gastrointestinal tract. Neuropeptides produced by the ENS play a crucial role in the regulation of inflammatory processes via cross talk with the enteric immune system. In addition, neuropeptides have paracrine effects on epithelial secretion, thus regulating epithelial barrier functions and thereby susceptibility to inflammation. Ultimately the inflammatory response damages the enteric neurons themselves, resulting in deregulations in circuitry and gut motility. In this review, we have emphasized the concept of neurogenic inflammation and the interaction between the enteric immune system and enteric nervous system, focusing on neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP). The alterations in the expression of NPY and VIP in inflammation and their significant roles in immunomodulation are discussed. We highlight the mechanism of action of these neuropeptides on immune cells, focusing on the key receptors as well as the intracellular signaling pathways that are activated to regulate the release of cytokines. In addition, we also examine the direct and indirect mechanisms of neuropeptide regulation of epithelial tight junctions and permeability, which are a crucial determinant of susceptibility to inflammation. Finally, we also discuss the potential of emerging neuropeptide-based therapies that utilize peptide agonists, antagonists, siRNA, oligonucleotides, and lentiviral vectors.

Neuroimmune signaling in regulation of intestinal ion transport

1994 ◽  
Vol 266 (2) ◽  
pp. G167-G178 ◽  
Author(s):  
H. J. Cooke
Keyword(s):  
Nervous System ◽  
Immune System ◽  
Epithelial Cells ◽  
Enteric Nervous System ◽  
Inflammatory Mediators ◽  
Neural Circuits ◽  
Selective Excitation ◽  
Response Threshold ◽  
Complex Interactions ◽  
Intestinal Ion Transport

Complex interactions between the enteric nervous system, the immune system, and the epithelium govern the transport rates of salt and water across the intestinal lining. Luminal antigens or bacterial products are detected by the immune system, which triggers a cascade of events associated with the release of inflammatory mediators. These mediators, by lowering the response threshold for transmission in some neural circuits, augment ongoing neural reflexes that promote secretion. Associated with these effects is a dampening of responses in other neural circuits innervating the mucosal effectors. Selective excitation and inhibition of the neural reflex circuitry coupled with direct actions of inflammatory mediators on epithelial cells result in stereotypical motility and secretory patterns that are characterized by strong muscular contractions, copious secretion, and diarrhea.

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 Microbiota and Hypertension: Role of the Sympathetic Nervous System and the Immune System

2020 ◽  
Author(s):  
Iñaki Robles-Vera ◽  
Marta Toral ◽  
Juan Duarte
Keyword(s):  
T Cells ◽  
Nervous System ◽  
Immune System ◽  
Sympathetic Nervous System ◽  
Gut Microbiota ◽  
Current Knowledge ◽  
Vascular Inflammation ◽  
T Helper 17 ◽  
Sympathetic Nervous

Abstract There are numerous studies indicating a direct association between hypertension and gut microbiota in both animal models and humans. In this review, we focused on the imbalance in the gut microbiota composition relative to healthy state or homeostasis, termed dysbiosis, associated with hypertension and discuss the current knowledge regarding how microbiota regulates blood pressure (BP), involving the sympathetic nervous system and the immune system. The profile of ecological parameters and bacterial genera composition of gut dysbiosis in hypertension varies according to the experimental model of hypertension. Recent evidence supports that gut microbiota can protect or promote the development of hypertension by interacting with gut secondary lymph organs and altering T helper 17/regulatory T cells polarization, with subsequent changes in T cells infiltration in vascular tissues. Here, we also describe the bidirectional communication between the microbiome and the host via the sympathetic nervous system and its role in BP regulation. Dysbiosis in hypertension is mainly associated with reduced proportions of short-chain fatty acid-producing bacteria, mainly acetate- and butyrate-producing bacteria, and an increased enrichment of the genes for lipopolysaccharide biosynthesis and export, lending to moderate endotoxemia. The role of these metabolic and structural products in both immune and sympathetic system regulation and vascular inflammation was also analyzed. Overall, gut microbiota is now recognized as a well-established target to dietary interventions with prebiotics or probiotics to reduce BP.

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