scholarly journals Gut Microbiota in Neurological Disorders

2019 ◽  
Vol 67 (6) ◽  
pp. 375-383 ◽  
Author(s):  
Marta Grochowska ◽  
Tomasz Laskus ◽  
Marek Radkowski

Abstract The incidence of neurological disorders such as multiple sclerosis (MS), Alzheimer’s disease (AD) and Parkinson’s disease (PD) is increasing throughout the world, but their pathogenesis remains unclear and successful treatment remains elusive. Bidirectional communications between the central nervous system and gut microbiota may play some role in the pathogenesis of the above disorders. Up to a thousand bacterial species reside in human intestine; they colonize the gut shortly after birth and remain for life. Numerous studies point to the role of microbiota composition in the development, course and treatment of MS, AD and PD.

2019 ◽  
Vol 28 (12) ◽  
pp. 1507-1527 ◽  
Author(s):  
Giovanni Schepici ◽  
Serena Silvestro ◽  
Placido Bramanti ◽  
Emanuela Mazzon

Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating, and degenerative disease that affects the central nervous system. A recent study showed that interaction between the immune system and the gut microbiota plays a crucial role in the development of MS. This review reports the clinical studies carried out in recent years that aimed to evaluate the composition of the microbiota in patients with relapsing–remitting MS (RR-MS). We also report what is available in the literature regarding the effectiveness of fecal microbiota transplantation and the role of the diet in restoring the intestinal bacterial population. Studies report that patients with RR-MS have a microbiota that, compared with healthy controls, has higher amounts of Pedobacteria, Flavobacterium, Pseudomonas, Mycoplana, Acinetobacter, Eggerthella, Dorea, Blautia, Streptococcus and Akkermansia. In contrast, MS patients have a microbiota with impoverished microbial populations of Prevotella, Bacteroides, Parabacteroides, Haemophilus, Sutterella, Adlercreutzia, Coprobacillus, Lactobacillus, Clostridium, Anaerostipes and Faecalibacterium. In conclusion, the restoration of the microbial population in patients with RR-MS appears to reduce inflammatory events and the reactivation of the immune system.


Author(s):  
Sundar Khadka ◽  
Seiichi Omura ◽  
Fumitaka Sato ◽  
Kazuto Nishio ◽  
Hideaki Kakeya ◽  
...  

We developed a prodrug type of curcumin, curcumin monoglucuronide (CMG), whose intravenous/intraperitoneal injection achieves a high serum concentration of free-form curcumin. Although curcumin has been reported to alter the gut microbiota and immune responses, it is unclear whether the altered microbiota could be associated with inflammation in immune-mediated diseases, such as multiple sclerosis (MS). We aimed to determine whether CMG administration could affect the gut microbiota at three anatomical sites (feces, ileal contents, and the ileal mucosa), leading to suppression of inflammation in the central nervous system (CNS) in an autoimmune model for MS, experimental autoimmune encephalomyelitis (EAE). We injected EAE mice with CMG, harvested the brains and spinal cords for histological analyses, and conducted microbiome analyses using 16S rRNA sequencing. CMG administration modulated EAE clinically and histologically, and altered overall microbiota compositions in feces and ileal contents, but not the ileal mucosa. Principal component analysis (PCA) of the microbiome showed that principal component (PC) 1 values in ileal contents, but not in feces, correlated with the clinical and histological EAE scores. On the other hand, when we analyzed the individual bacteria of the microbiota, the EAE scores correlated with significant increases in the relative abundance of two bacterial species at each anatomical site: Ruminococcus bromii and Blautia (Ruminococcus) gnavus in feces, Turicibacter sp. and Alistipes finegoldii in ileal contents, and Burkholderia spp. and Azoarcus spp. in the ileal mucosa. Therefore, CMG administration could alter the gut microbiota at the three different sites differentially in not only the overall gut microbiome compositions but also the abundance of individual bacteria, each of which was associated with modulation of neuroinflammation.


2021 ◽  
Vol 19 ◽  
Author(s):  
Xu Wang ◽  
Zhen Liang ◽  
Shengnan Wang ◽  
Di Ma ◽  
Mingqin Zhu ◽  
...  

: The role of gut microbiota in health and diseases has been receiving increased attention recently. Emerging evidence from previous studies on the gut-microbiota-brain axis highlighted the importance of gut microbiota in neurological disorders. Multiple sclerosis (MS) is a chronic, inflammatory, demyelinating disease of the central nervous system (CNS) resulting from T-cell-driven, myelin-directed autoimmunity. The dysbiosis of gut microbiota in MS patients has been reported in published research studies, indicating that gut microbiota plays an important role in the pathogenesis of MS. Gut microbiota has also been reported to influence the initiation of disease and severity of experimental autoimmune encephalomyelitis, which is the animal model of MS. However, the underlying mechanisms of gut microbiota involvement in the pathogenesis of MS remain unclear. Therefore, in this review, we summerized the potential mechanisms for gut microbiota involvement in the pathogenesis of MS, including increasing the permeability of the intestinal barrier, initiating an autoimmune response, disrupting the blood-brain barrier integrity, and contributing to chronic inflammation. The possibility for gut microbiota as a target for MS therapy has also been discussed. This review provides new insight into understanding the role of gut microbiota in neurological and inflammatory diseases.


2021 ◽  
Vol 22 (9) ◽  
pp. 4692
Author(s):  
Anna Ferrulli ◽  
Lorenzo Drago ◽  
Sara Gandini ◽  
Stefano Massarini ◽  
Federica Bellerba ◽  
...  

Growing evidence highlights the crucial role of gut microbiota in affecting different aspects of obesity. Considering the ability of deep transcranial magnetic stimulation (dTMS) to modulate the cortical excitability, the reward system, and, indirectly, the autonomic nervous system (ANS), we hypothesized a potential role of dTMS in affecting the brain-gut communication pathways, and the gut microbiota composition in obesity. In a hospital setting, 22 subjects with obesity (5 M, 17 F; 44.9 ± 2.2 years; BMI 37.5 ± 1.0 kg/m2) were randomized into three groups receiving 15 sessions (3 per week for 5 weeks) of high frequency (HF), low frequency (LF) dTMS, or sham stimulation. Fecal samples were collected at baseline and after 5 weeks of treatment. Total bacterial DNA was extracted from fecal samples using the QIAamp DNA Stool Mini Kit (Qiagen, Italy) and analyzed by a metagenomics approach (Ion Torrent Personal Genome Machine). After 5 weeks, a significant weight loss was found in HF (HF: −4.1 ± 0.8%, LF: −1.9 ± 0.8%, sham: −1.3 ± 0.6%, p = 0.042) compared to LF and sham groups, associated with a decrease in norepinephrine compared to baseline (HF: −61.5 ± 15.2%, p < 0.01; LF: −31.8 ± 17.1%, p < 0.05; sham: −35.8 ± 21.0%, p > 0.05). Furthermore, an increase in Faecalibacterium (+154.3% vs. baseline, p < 0.05) and Alistipes (+153.4% vs. baseline, p < 0.05) genera, and a significant decrease in Lactobacillus (−77.1% vs. baseline, p < 0.05) were found in HF. Faecalibacterium variations were not significant compared to baseline in the other two groups (LF: +106.6%, sham: +27.6%; p > 0.05) as well as Alistipes (LF: −54.9%, sham: −15.1%; p > 0.05) and Lactobacillus (LF: −26.0%, sham: +228.3%; p > 0.05) variations. Norepinephrine change significantly correlated with Bacteroides (r2 = 0.734; p < 0.05), Eubacterium (r2 = 0.734; p < 0.05), and Parasutterella (r2 = 0.618; p < 0.05) abundance variations in HF. In conclusion, HF dTMS treatment revealed to be effective in modulating gut microbiota composition in subjects with obesity, reversing obesity-associated microbiota variations, and promoting bacterial species representative of healthy subjects with anti-inflammatory properties.


2021 ◽  
Vol 22 (11) ◽  
pp. 5576
Author(s):  
Jana Amlerova ◽  
Jan Šroubek ◽  
Francesco Angelucci ◽  
Jakub Hort

Epilepsy as a chronic neurological disorder is characterized by recurrent, unprovoked epileptic seizures. In about half of the people who suffer from epilepsy, the root cause of the disorder is unknown. In the other cases, different factors can cause the onset of epilepsy. In recent years, the role of gut microbiota has been recognized in many neurological disorders, including epilepsy. These data are based on studies of the gut microbiota–brain axis, a relationship starting by a dysbiosis followed by an alteration of brain functions. Interestingly, epileptic patients may show signs of dysbiosis, therefore the normalization of the gut microbiota may lead to improvement of epilepsy and to greater efficacy of anticonvulsant drugs. In this descriptive review, we analyze the evidences for the role of gut microbiota in epilepsy and hypothesize a mechanism of action of these microorganisms in the pathogenesis and treatment of the disease. Human studies revealed an increased prevalence of Firmicutes in patients with refractory epilepsy. Exposure to various compounds can change microbiota composition, decreasing or exacerbating epileptic seizures. These include antibiotics, epileptic drugs, probiotics and ketogenic diet. Finally, we hypothesize that physical activity may play a role in epilepsy through the modulation of the gut microbiota.


2021 ◽  
Vol 12 ◽  
Author(s):  
Austin P. Passaro ◽  
Abraham L. Lebos ◽  
Yao Yao ◽  
Steven L. Stice

Neuroinflammation is a key component of neurological disorders and is an important therapeutic target; however, immunotherapies have been largely unsuccessful. In cases where these therapies have succeeded, particularly multiple sclerosis, they have primarily focused on one aspect of the disease and leave room for improvement. More recently, the impact of the peripheral immune system is being recognized, since it has become evident that the central nervous system is not immune-privileged, as once thought. In this review, we highlight key interactions between central and peripheral immune cells in neurological disorders. While traditional approaches have examined these systems separately, the immune responses and processes in neurological disorders consist of substantial crosstalk between cells of the central and peripheral immune systems. Here, we provide an overview of major immune effector cells and the role of the blood-brain barrier in regard to neurological disorders and provide examples of this crosstalk in various disorders, including stroke and traumatic brain injury, multiple sclerosis, neurodegenerative diseases, and brain cancer. Finally, we propose targeting central-peripheral immune interactions as a potential improved therapeutic strategy to overcome failures in clinical translation.


2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S39-S40
Author(s):  
Victoria Godfrey ◽  
Hasan Zaki

Abstract The incidence of inflammatory bowel disease (IBD) is strikingly high in Western countries, implicating the role of Western diet in its etiology and pathogenesis. Western diet is characterized by high fat, low fiber, and high sugar. Despite clinical evidence of an association between high sugar diet and IBD susceptibility, the precise role of dietary simple sugars such as glucose, fructose, and sucrose in colitis pathogenesis is unknown. Using dextran sodium sulfate (DSS) and IL10-deficient mouse models of colitis, we studied the effect of simple sugars in colitis susceptibility. Mice were given high glucose, fructose or sucrose in their drinking water or left untreated before and during colitis induced by DSS. Sugar-fed mice exhibited increased colitis susceptibility evidenced by higher body weight loss, diarrhea, rectal bleeding, and severe histopathological changes in the colon as compared to those of sugar-untreated colitic mice. Pre-colitis dietary habit of sugar consumption was critical since sugar pretreated mice were susceptible to DSS-induced colitis even without high sugar diet intake during DSS administration. Consistent with these findings, there were higher incidence of spontaneous colitis development in Il10-/- mice following consumption of high sugar. To understand the underlying mechanism, we evaluated the effect of high sugar diet on intestinal epithelial cell death, inflammation, epithelial barrier permeability, and gut microbiota composition in healthy mice. We did not observe any major pathological changes and apoptosis in the colon of sugar-fed mice. Inflammatory responses, activation of inflammatory signaling pathways, and the expression of tight junction proteins were comparable between control and sugar-fed mice. Interestingly, gut microbiota composition of sugar-fed mice was altered as measured by 16S rRNA gene sequencing of DNA isolated from feces. Microbial species richness was reduced and relative abundance of several bacterial species was either increased or decreased in sugar-fed mice. We further confirmed that sugar-induced alteration of gut microbiota is responsible for exacerbated colitis by using antibiotics or germ-free mice. Mice receiving antibiotics during high-sugar intake did not show increased DSS-colitis susceptibility. Similarly, high-sugar diet did not induce overt colitis pathogenesis in germ-free mice. These findings demonstrate a critical role of dietary caloric sugars in the predisposition and promotion of colitis and could be implicated in the treatment and management of IBD.


Nutrients ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 644 ◽  
Author(s):  
Iryna Liauchonak ◽  
Bessi Qorri ◽  
Fady Dawoud ◽  
Yatin Riat ◽  
Myron Szewczuk

Individuals widely use non-nutritive sweeteners (NNS) in attempts to lower their overall daily caloric intake, lose weight, and sustain a healthy diet. There are insufficient scientific data that support the safety of consuming NNS. However, recent studies have suggested that NNS consumption can induce gut microbiota dysbiosis and promote glucose intolerance in healthy individuals that may result in the development of type 2 diabetes mellitus (T2DM). This sequence of events may result in changes in the gut microbiota composition through microRNA (miRNA)-mediated changes. The mechanism(s) by which miRNAs alter gene expression of different bacterial species provides a link between the consumption of NNS and the development of metabolic changes. Another potential mechanism that connects NNS to metabolic changes is the molecular crosstalk between the insulin receptor (IR) and G protein-coupled receptors (GPCRs). Here, we aim to highlight the role of NNS in obesity and discuss IR-GPCR crosstalk and miRNA-mediated changes, in the manipulation of the gut microbiota composition and T2DM pathogenesis.


2021 ◽  
Vol 12 (1) ◽  
pp. 1-3 ◽  
Author(s):  
Koen Venema

At the start of 2020 we were thrilled to have reached 10 years of Beneficial Microbes! Little did we know that soon after Europe and the rest of the world (with Asia already earlier) would be in lock-down due to COVID-19. It has been a strange year. And now, at the start of 2021, the excitement of having a vaccine is tempered by the fact that everywhere mutants of the virus pop up. Although this was likely to occur, as also the influenza virus keeps mutating, it means that at the moment it is unclear as to whether the current situation of lock-downs and social distancing will remain for a longer period than we had anticipated and hoped for at the end of 2020 when it became clear that several vaccines were efficacious. Some studies have shown a role of the gut microbiota composition in disease severity, together with vitamin D, cholesterol and other factors. It was a hype to write a ‘review’ on gut microbiota and the effect on COVID-19, and also the board of Beneficial Microbes has received several submissions of so-called reviews on the topic. However, all of them were rejected, as they were mere speculations about how the gut microbiota might affect virus infection and disease severity, without any data whatsoever. However, there are some good studies out there that have shown that a proper gut microbiota may indeed influence disease severity, such as recently reviewed by Kim (2021). All in all, this may not be too surprising for the knowledgeable reader, as they would know that the microbiota plays a role in everything that can be wrong with us!


2020 ◽  
Vol 21 (20) ◽  
pp. 7551
Author(s):  
Kanmani Suganya ◽  
Byung-Soo Koo

The gut microbiome acts as an integral part of the gastrointestinal tract (GIT) that has the largest and vulnerable surface with desirable features to observe foods, nutrients, and environmental factors, as well as to differentiate commensals, invading pathogens, and others. It is well-known that the gut has a strong connection with the central nervous system (CNS) in the context of health and disease. A healthy gut with diverse microbes is vital for normal brain functions and emotional behaviors. In addition, the CNS controls most aspects of the GI physiology. The molecular interaction between the gut/microbiome and CNS is complex and bidirectional, ensuring the maintenance of gut homeostasis and proper digestion. Besides this, several mechanisms have been proposed, including endocrine, neuronal, toll-like receptor, and metabolites-dependent pathways. Changes in the bidirectional relationship between the GIT and CNS are linked with the pathogenesis of gastrointestinal and neurological disorders; therefore, the microbiota/gut-and-brain axis is an emerging and widely accepted concept. In this review, we summarize the recent findings supporting the role of the gut microbiota and immune system on the maintenance of brain functions and the development of neurological disorders. In addition, we highlight the recent advances in improving of neurological diseases by probiotics/prebiotics/synbiotics and fecal microbiota transplantation via the concept of the gut–brain axis.


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