scholarly journals Neuroimmune Interactions in the Gut and Their Significance for Intestinal Immunity

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 670 ◽  
Author(s):  
David J. Brinkman ◽  
Anne S. ten Hove ◽  
Margriet J. Vervoordeldonk ◽  
Misha D. Luyer ◽  
Wouter J. de Jonge

Inflammatory bowel diseases (IBD) have a complex, multifactorial pathophysiology with an unmet need for effective treatment. This calls for novel strategies to improve disease outcome and quality of life for patients. Increasing evidence suggests that autonomic nerves and neurotransmitters, as well as neuropeptides, modulate the intestinal immune system, and thereby regulate the intestinal inflammatory processes. Although the autonomic nervous system is classically divided in a sympathetic and parasympathetic branch, both play a pivotal role in the crosstalk with the immune system, with the enteric nervous system acting as a potential interface. Pilot clinical trials that employ vagus nerve stimulation to reduce inflammation are met with promising results. In this paper, we review current knowledge on the innervation of the gut, the potential of cholinergic and adrenergic systems to modulate intestinal immunity, and comment on ongoing developments in clinical trials.

2019 ◽  
Vol 20 (8) ◽  
pp. 799-816 ◽  
Author(s):  
Yue Qiu ◽  
Guo-wei Tu ◽  
Min-jie Ju ◽  
Cheng Yang ◽  
Zhe Luo

Sepsis, which is a highly heterogeneous syndrome, can result in death as a consequence of a systemic inflammatory response syndrome. The activation and regulation of the immune system play a key role in the initiation, development and prognosis of sepsis. Due to the different periods of sepsis when the objects investigated were incorporated, clinical trials often exhibit negative or even contrary results. Thus, in this review we aim to sort out the current knowledge in how immune cells play a role during sepsis.


2013 ◽  
Vol 304 (11) ◽  
pp. G949-G957 ◽  
Author(s):  
Bindu Chandrasekharan ◽  
Behtash Ghazi Nezami ◽  
Shanthi Srinivasan

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.


1997 ◽  
Vol 6 (5-6) ◽  
pp. 303-309 ◽  
Author(s):  
J. D. Van Bergeijk ◽  
J. H. P. Wilson

Intestinal inflammation is controlled by various immunomodulating cells, interacting by molecular mediators. Neuropeptides, released by enteric nerve cells and neuroendocrine mucosa cells, are able to affect several aspects of the general and intestinal immune system, with both pro- as well as anti-inflammatory activities. In inflammatory bowel disease (IBD) there is both morphological as well as experimental evidence for involvement of neuropeptides in the pathogenesis. Somatostatin is the main inhibitory peptide in inflammatory processes, and its possible role in IBD is discussed.


Author(s):  
Iñaki Robles-Vera ◽  
Marta Toral ◽  
Juan Duarte

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.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Simona Frosali ◽  
Danilo Pagliari ◽  
Giovanni Gambassi ◽  
Raffaele Landolfi ◽  
Franco Pandolfi ◽  
...  

The gut is able to maintain tolerance to microbial and food antigens. The intestine minimizes the number of harmful bacteria by shaping the microbiota through a symbiotic relationship. In healthy human intestine, a constant homeostasis is maintained by the perfect regulation of microbial load and the immune response generated against it. Failure of this balance may result in various pathological conditions. Innate immune sensors, such as Toll-like receptors (TLRs), may be considered an interface among intestinal epithelial barrier, microbiota, and immune system. TLRs pathway, activated by pathogens, is involved in the pathogenesis of several infectious and inflammatory diseases. The alteration of the homeostasis between physiologic and pathogenic bacteria of intestinal flora causes a condition called dysbiosis. The breakdown of homeostasis by dysbiosis may increase susceptibility to inflammatory bowel diseases. It is evident that environment, genetics, and host immunity form a highly interactive regulatory triad that controls TLR function. Imbalanced relationships within this triad may promote aberrant TLR signaling, critically contributing to acute and chronic intestinal inflammatory processes, such as in IBD, colitis, and colorectal cancer. The study of interactions between different components of the immune systems and intestinal microbiota will open new horizons in the knowledge of gut inflammation.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1507
Author(s):  
Mercedes Lopez-Santalla ◽  
Marina Inmaculada Garin

Inflammatory bowel diseases (IBD) consisting of persistent and relapsing inflammatory processes of the intestinal mucosa are caused by genetic, environmental, and commensal microbiota factors. Despite recent advances in clinical treatments aiming to decrease inflammation, nearly 30% of patients treated with biologicals experienced drawbacks including loss of response, while others can develop severe side effects. Hence, novel effective treatments are highly needed. Mesenchymal stem/stromal cell (MSCs) therapy is an innovative therapeutic alternative currently under investigation for IBD. MSCs have the inherent capacity of modulating inflammatory immune responses as well as regenerating damaged tissues and are therefore a prime candidate to use as cell therapy in patients with IBD. At present, MSC-based therapy has been shown preclinically to modulate intestinal inflammation, whilst the safety of MSC-based therapy has been demonstrated in clinical trials. However, the successful results in preclinical studies have not been replicated in clinical trials. In this review, we will summarize the protocols used in preclinical and clinical trials and the novel approaches currently under investigation which aim to increase the beneficial effects of MSC-based therapy for IBD.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Saad Khan ◽  
Helen Luck ◽  
Shawn Winer ◽  
Daniel A. Winer

AbstractThe intestinal immune system is an important modulator of glucose homeostasis and obesity-associated insulin resistance. Dietary factors, the intestinal microbiota and their metabolites shape intestinal immunity during obesity. The intestinal immune system in turn affects processes such as intestinal permeability, immune cell trafficking, and intestinal hormone availability, impacting systemic insulin resistance. Understanding these pathways might identify mechanisms underlying treatments for insulin resistance, such as metformin and bariatric surgery, or aid in developing new therapies and vaccination approaches. Here, we highlight evolving concepts centered on intestinal immunity, diet, and the microbiota to provide a working model of obesity-related metabolic disease.


2008 ◽  
Vol 2 ◽  
pp. CCRPM.S547 ◽  
Author(s):  
Peyman Otmishi ◽  
Joshiah Gordon ◽  
Seraj El-Oshar ◽  
Huafeng Li ◽  
Juan Guardiola ◽  
...  

The inflammatory response is modulated through interactions among the nervous, endocrine, and immune systems. Intercommunication between immune cells and the autonomic nervous system is a growing area of interest. Spatial and temporal information about inflammatory processes is relayed to the central nervous system (CNS) where neuroimmune modulation serves to control the extent and intensity of the inflammation. Over the past few decades, research has revealed various routes by which the nervous system and the immune system communicate. The CNS regulates the immune system via hormonal and neuronal pathways, including the sympathetic and parasympathetic nerves. The immune system signals the CNS through cytokines that act both centrally and peripherally. This review aims to introduce the concept of neuroimmune interaction and discuss its potential clinical application, in an attempt to broaden the awareness of this rapidly evolving area and open up new avenues that may aid in the treatment of inflammatory diseases.


2020 ◽  
pp. 92-100
Author(s):  
E. A. Kornienko

Introduction. The intestinal microbiome is an integral part of the health of its owner and performs several important functions: metabolic, coordinating, protective, epigenetic, which are closely interactive. In conditions of dysbiosis, disturbances of these functions contributes to different disorders.The intestinal immune system closely interacts with the microbiota. It is represented by all cells: T- and B-lymphocytes, T-regulatory, dendritic cells, macrophages. Micropresentation of antigens occurs through M-cells located between enterocytes. Toll-like receptors that recognize bacterial patterns are presented on the epithelial membrane. Dendritic cells present these antigens to T-cells and direct a further adaptive immune response.The immune system matures as a result of colonization of the intestine with microbiota, which is confirmed experimentally in gnotobiotic animals. Under physiological conditions, the immune system provides tolerance to its own microbiota through Tr-cells. Tolerogenic effects decrease in dysbiotic conditions, as a result, inflammation develops.The state of the intestinal barrier. The intestinal barrier is maintained by microbiota, which stimulates the synthesis of mucin and claudine. In dysbiosis, permeability increases, and the immune system is attacked by microbes and their metabolites, which contributes to inflammation.Dysbiosis predisposes to the development of inflammatory bowel diseases, colorectal cancer, metabolic syndrome and obesity, food allergies. In these diseases, the microbiota loses its diversity and richness and has a predominantly pro-inflammatory effect.The effect of probiotics on the immune system. Probiotics, due to adhesion to the mucous layer, enhance barrier functions, interact with the immune system, affect dendritic cells, promoting the formation of Tr and inhibiting the activation of NF-kB. Commensal metabolites (butyrate) increase the involvement of Tr cells in the colon, exerting a tolerogenic effect.Indications for the appointment of probiotics. Enterococcus faecium and Bifidobacterium longum have proven their activities similar to normal microbiota, and effectiveness in treatment of dysbiosis in children and adults.


Sign in / Sign up

Export Citation Format

Share Document