scholarly journals Adiponectin Role in Neurodegenerative Diseases: Focus on Nutrition Review

2020 ◽  
Vol 21 (23) ◽  
pp. 9255
Author(s):  
Rita Polito ◽  
Irene Di Meo ◽  
Michelangela Barbieri ◽  
Aurora Daniele ◽  
Giuseppe Paolisso ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Neurodegenerative Diseases ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Metabolic Effects ◽  
Beneficial Effects ◽  
The Central Nervous System ◽  
Regulatory Effects ◽  
Nutrition Review ◽  
Selective Process

Adiponectin is an adipokine produced by adipose tissue. It has numerous beneficial effects. In particular, it improves metabolic effects and glucose homeostasis, lipid profile, and is involved in the regulation of cytokine profile and immune cell production, having anti-inflammatory and immune-regulatory effects. Adiponectin’s role is already known in immune diseases and also in neurodegenerative diseases. Neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, are a set of diseases of the central nervous system, characterized by a chronic and selective process of neuron cell death, which occurs mainly in relation to oxidative stress and neuroinflammation. Lifestyle is able to influence the development of these diseases. In particular, unhealthy nutrition on gut microbiota, influences its composition and predisposition to develop many diseases such as neurodegenerative diseases, given the importance of the “gut-brain” axis. There is a strong interplay between Adiponectin, gut microbiota, and brain-gut axis. For these reasons, a healthy diet composed of healthy nutrients such as probiotics, prebiotics, polyphenols, can prevent many metabolic and inflammatory diseases such as neurodegenerative diseases and obesity. The special Adiponectin role should be taken into account also, in order to be able to use this component as a therapeutic molecule.

scholarly journals Regulation of Energy Expenditure and Brown/Beige Thermogenic Activity by Interleukins: New Roles for Old Actors

2018 ◽  
Vol 19 (9) ◽  
pp. 2569 ◽  
Author(s):  
María García ◽  
Patricia Pazos ◽  
Luis Lima ◽  
Carlos Diéguez
Keyword(s):  
Energy Expenditure ◽  
Immune Cell ◽  
Therapeutic Potential ◽  
Molecular Switches ◽  
Metabolic Effects ◽  
Signalling Pathways ◽  
Functional Heterogeneity ◽  
Beige Adipocytes ◽  
The Central Nervous System ◽  
And Function

Obesity rates and the burden of metabolic associated diseases are escalating worldwide Energy burning brown and inducible beige adipocytes in human adipose tissues (ATs) have attracted considerable attention due to their therapeutic potential to counteract the deleterious metabolic effects of nutritional overload and overweight. Recent research has highlighted the relevance of resident and recruited ATs immune cell populations and their signalling mediators, cytokines, as modulators of the thermogenic activity of brown and beige ATs. In this review, we first provide an overview of the developmental, cellular and functional heterogeneity of the AT organ, as well as reported molecular switches of its heat-producing machinery. We also discuss the key contribution of various interleukins signalling pathways to energy and metabolic homeostasis and their roles in the biogenesis and function of brown and beige adipocytes. Besides local actions, attention is also drawn to their influence in the central nervous system (CNS) networks governing energy expenditure.

scholarly journals Molecular patterns from a human gut-derived Lactobacillus strain suppress pathogenic infiltration of leukocytes into the central nervous system

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
John Michael S. Sanchez ◽  
Daniel J. Doty ◽  
Ana Beatriz DePaula-Silva ◽  
D. Garrett Brown ◽  
Rickesha Bell ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gut Microbiota ◽  
Immune Cell ◽  
Cell Infiltration ◽  
Immune Cell Infiltration ◽  
Human Gut ◽  
Chemokine Production ◽  
The Central Nervous System ◽  
Molecular Patterns

Abstract Background Multiple sclerosis (MS) is an inflammatory demyelinating disease that affects 2.5 million people worldwide. Growing evidence suggests that perturbation of the gut microbiota, the dense collection of microorganisms that colonize the gastrointestinal tract, plays a functional role in MS. Indeed, specific gut-resident bacteria are altered in patients with MS compared to healthy individuals, and colonization of gnotobiotic mice with MS-associated microbiota exacerbates preclinical models of MS. However, defining the molecular mechanisms by which gut commensals can remotely affect the neuroinflammatory process remains a critical gap in the field. Methods We utilized monophasic experimental autoimmune encephalomyelitis (EAE) in C57BL/6J mice and relapse-remitting EAE in SJL/J mice to test the effects of the products from a human gut-derived commensal strain of Lactobacillus paracasei (Lb). Results We report that Lb can ameliorate preclinical murine models of MS with both prophylactic and therapeutic administrations. Lb ameliorates disease through a Toll-like receptor 2-dependent mechanism via its microbe-associated molecular patterns that can be detected in the systemic circulation, are sufficient to downregulate chemokine production, and can reduce immune cell infiltration into the central nervous system (CNS). In addition, alterations in the gut microbiota mediated by Lb-associated molecular patterns are sufficient to provide partial protection against neuroinflammatory diseases. Conclusions Local Lb modulation of the gut microbiota and the shedding of Lb-associated molecular patterns into the circulation may be important physiological signals to prevent aberrant peripheral immune cell infiltration into the CNS and have relevance to the development of new therapeutic strategies for MS.

scholarly journals The Potential Effects of Probiotics and ω-3 Fatty Acids on Chronic Low-Grade Inflammation

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2402 ◽  
Author(s):  
Ashley N. Hutchinson ◽  
Lina Tingö ◽  
Robert Jan Brummer
Keyword(s):  
Fatty Acids ◽  
Gut Microbiota ◽  
Cell Function ◽  
Immune Cell ◽  
Low Grade ◽  
Beneficial Effects ◽  
Positive Effects ◽  
Immune Mediators ◽  
Low Grade Inflammation ◽  
Microbiota Diversity

Chronic low-grade inflammation negatively impacts health and is associated with aging and obesity, among other health outcomes. A large number of immune mediators are present in the digestive tract and interact with gut bacteria to impact immune function. The gut microbiota itself is also an important initiator of inflammation, for example by releasing compounds such as lipopolysaccharides (LPS) that may influence cytokine production and immune cell function. Certain nutrients (e.g., probiotics, ω-3 fatty acids [FA]) may increase gut microbiota diversity and reduce inflammation. Lactobacilli and Bifidobacteria, among others, prevent gut hyperpermeability and lower LPS-dependent chronic low-grade inflammation. Furthermore, ω-3 FA generate positive effects on inflammation-related conditions (e.g., hypertriglyceridemia, diabetes) by interacting with immune, metabolic, and inflammatory pathways. Ω-3 FA also increase LPS-suppressing bacteria (i.e., Bifidobacteria) and decrease LPS-producing bacteria (i.e., Enterobacteria). Additionally, ω-3 FA appear to promote short-chain FA production. Therefore, combining probiotics with ω-3 FA presents a promising strategy to promote beneficial immune regulation via the gut microbiota, with potential beneficial effects on conditions of inflammatory origin, as commonly experienced by aged and obese individuals, as well as improvements in gut-brain-axis communication.

Role of Gut Microbiota in Multiple Sclerosis and Potential Therapeutic Implications

2021 ◽  
Vol 19 ◽  
Author(s):  
Xu Wang ◽  
Zhen Liang ◽  
Shengnan Wang ◽  
Di Ma ◽  
Mingqin Zhu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Gut Microbiota ◽  
Demyelinating Disease ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Autoimmune Response ◽  
Therapeutic Implications ◽  
The Central Nervous System ◽  
Underlying Mechanisms

: 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.

scholarly journals The Central Role of the Gut Microbiota in Chronic Inflammatory Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Caroline Marcantonio Ferreira ◽  
Angélica Thomaz Vieira ◽  
Marco Aurelio Ramirez Vinolo ◽  
Fernando A. Oliveira ◽  
Rui Curi ◽  
...  
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Sequencing Analysis ◽  
Metagenomic Sequencing ◽  
Microbiota Composition ◽  
Chronic Inflammatory Diseases ◽  
Commensal Microbiota

The commensal microbiota is in constant interaction with the immune system, teaching immune cells to respond to antigens. Studies in mice have demonstrated that manipulation of the intestinal microbiota alters host immune cell homeostasis. Additionally, metagenomic-sequencing analysis has revealed alterations in intestinal microbiota in patients suffering from inflammatory bowel disease, asthma, and obesity. Perturbations in the microbiota composition result in a deficient immune response and impaired tolerance to commensal microorganisms. Due to altered microbiota composition which is associated to some inflammatory diseases, several strategies, such as the administration of probiotics, diet, and antibiotic usage, have been utilized to prevent or ameliorate chronic inflammatory diseases. The purpose of this review is to present and discuss recent evidence showing that the gut microbiota controls immune system function and onset, development, and resolution of some common inflammatory diseases.

scholarly journals Gut Microbiota-Modulated Metabolomic Profiling Shapes the Etiology and Pathogenesis of Autoimmune Diseases

2021 ◽  
Vol 9 (9) ◽  
pp. 1930
Author(s):  
Yi-Wen Tsai ◽  
Jia-Ling Dong ◽  
Yun-Jie Jian ◽  
Shin-Huei Fu ◽  
Ming-Wei Chien ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Autoimmune Diseases ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Functional Decline ◽  
Intestinal Microbiome ◽  
Health Concern ◽  
Multiple Organs ◽  
Immunological Homeostasis ◽  
Gut Microbial Community

Autoimmunity is a complex and multifaceted process that contributes to widespread functional decline that affects multiple organs and tissues. The pandemic of autoimmune diseases, which are a global health concern, augments in both the prevalence and incidence of autoimmune diseases, including type 1 diabetes, multiple sclerosis, and rheumatoid arthritis. The development of autoimmune diseases is phenotypically associated with gut microbiota-modulated features at the molecular and cellular levels. The etiology and pathogenesis of autoimmune diseases comprise the alterations of immune systems with the innate and adaptive immune cell infiltration into specific organs and the augmented production of proinflammatory cytokines stimulated by commensal microbiota. However, the relative importance and mechanistic interrelationships between the gut microbial community and the immune system during progression of autoimmune diseases are still not well understood. In this review, we describe studies on the profiling of gut microbial signatures for the modulation of immunological homeostasis in multiple inflammatory diseases, elucidate their critical roles in the etiology and pathogenesis of autoimmune diseases, and discuss the implications of these findings for these disorders. Targeting intestinal microbiome and its metabolomic associations with the phenotype of autoimmunity will enable the progress of developing new therapeutic strategies to counteract microorganism-related immune dysfunction in these autoimmune diseases.

scholarly journals Overview of Beneficial Effects of (Poly)phenol Metabolites in the Context of Neurodegenerative Diseases on Model Organisms

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2940
Author(s):  
Diogo Carregosa ◽  
Sara Mota ◽  
Sofia Ferreira ◽  
Beatriz Alves-Dias ◽  
Natasa Loncarevic-Vasiljkovic ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Gut Microbiota ◽  
Neurodegenerative Diseases ◽  
Intervention Studies ◽  
Economic Consequences ◽  
Model Organisms ◽  
Low Molecular Weight ◽  
Beneficial Effects ◽  
Critical Insight

The rise of neurodegenerative diseases in an aging population is an increasing problem of health, social and economic consequences. Epidemiological and intervention studies have demonstrated that diets rich in (poly)phenols can have potent health benefits on cognitive decline and neurodegenerative diseases. Meanwhile, the role of gut microbiota is ever more evident in modulating the catabolism of (poly)phenols to dozens of low molecular weight (poly)phenol metabolites that have been identified in plasma and urine. These metabolites can reach circulation in higher concentrations than parent (poly)phenols and persist for longer periods of time. However, studies addressing their potential brain effects are still lacking. In this review, we will discuss different model organisms that have been used to study how low molecular weight (poly)phenol metabolites affect neuronal related mechanisms gathering critical insight on their potential to tackle the major hallmarks of neurodegeneration.

scholarly journals Influence of Resveratrol on the Immune Response

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 946 ◽  
Author(s):  
Malaguarnera
Keyword(s):  
Immune Cell ◽  
Inflammatory Diseases ◽  
Adenosine Monophosphate ◽  
Nuclear Factor Κb ◽  
Biologically Active ◽  
Cellular Processes ◽  
Genes Expression ◽  
Anti Oxidant ◽  
Regulatory Effects ◽  
Systematic Understanding

Resveratrol is the most well-known polyphenolic stilbenoid, present in grapes, mulberries, peanuts, rhubarb, and in several other plants. Resveratrol can play a beneficial role in the prevention and in the progression of chronic diseases related to inflammation such as diabetes, obesity, cardiovascular diseases, neurodegeneration, and cancers among other conditions. Moreover, resveratrol regulates immunity by interfering with immune cell regulation, proinflammatory cytokines’ synthesis, and gene expression. At the molecular level, it targets sirtuin, adenosine monophosphate kinase, nuclear factor-κB, inflammatory cytokines, anti-oxidant enzymes along with cellular processes such as gluconeogenesis, lipid metabolism, mitochondrial biogenesis, angiogenesis, and apoptosis. Resveratrol can suppress the toll-like receptor (TLR) and pro-inflammatory genes’ expression. The antioxidant activity of resveratrol and the ability to inhibit enzymes involved in the production of eicosanoids contribute to its anti-inflammation properties. The effects of this biologically active compound on the immune system are associated with widespread health benefits for different autoimmune and chronic inflammatory diseases. This review offers a systematic understanding of how resveratrol targets multiple inflammatory components and exerts immune-regulatory effects on immune cells.

scholarly journals Protective Effects of SPA0355, a Thiourea Analogue, Against Lipopolysaccharide-Induced Acute Kidney Injury in Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 585 ◽  
Author(s):  
Jung-Yeon Kim ◽  
Jaechan Leem ◽  
Hyo-Lim Hong
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Cell Apoptosis ◽  
Immune Cell ◽  
Inflammatory Diseases ◽  
Kidney Injury ◽  
Tubular Cell ◽  
Protective Effects ◽  
Beneficial Effects ◽  
P53 Signaling

Inflammation and oxidative stress plays an essential role in the pathophysiology of sepsis-associated acute kidney injury (AKI). SPA0355, a thiourea analogue, has been shown to display beneficial effects against a variety of inflammatory diseases arising from its anti-inflammatory and anti-oxidant properties. However, the potential protective effects of SPA0355 against lipopolysaccharide (LPS)-induced AKI have not been explored. The aim of this study was to evaluate the effects of SPA0355 on LPS-induced AKI and investigate its underlying mechanisms. We found that renal dysfunction and histological abnormalities after LPS injection were significantly ameliorated by SPA0355. The compound also reduced renal expression of tubular injury markers. Mechanistically, SPA0355 significantly suppressed plasma and tissue levels of inflammatory cytokines and immune cell infiltration with inhibition of nuclear factor kappa-B p65 signaling. In addition, elevated levels of 4-hydroxynonenal and malondialdehyde after LPS injection were significantly decreased by SPA0355. The compound also regulated expression of pro-oxidant and antioxidant enzymes after LPS injection. Moreover, SPA0355 attenuated LPS-induced tubular cell apoptosis via inhibition of p53 signaling pathway. Altogether, these results suggest that SPA0355 protects against LPS-induced AKI through suppressing inflammation, oxidative stress, and tubular cell apoptosis and might be a potential preventive option for the disease.

scholarly journals 2′-Fucosyllactose Supplementation Improves Gut-Brain Signaling and Diet-Induced Obese Phenotype and Changes the Gut Microbiota in High Fat-Fed Mice

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1003 ◽  
Author(s):  
Sunhye Lee ◽  
Michael Goodson ◽  
Wendie Vang ◽  
Karen Kalanetra ◽  
Daniela Barile ◽  
...  
Keyword(s):  
Body Weight ◽  
Gut Microbiota ◽  
Energy Intake ◽  
Body Weight Gain ◽  
Metabolic Effects ◽  
Peroxisome Proliferator ◽  
High Fat ◽  
Gene Expressions ◽  
Beneficial Effects ◽  
Obese Phenotype

Obesity is characterized by fat accumulation, chronic inflammation and impaired satiety signaling, which may be due in part to gut microbial dysbiosis. Manipulations of the gut microbiota and its metabolites are attractive targets for obesity treatment. The predominant oligosaccharide found in human milk, acts as a prebiotic with beneficial effects on the host. However, little is known about the beneficial effects of 2′-FL in obesity. The aim of this study was to determine the beneficial effects of 2′-FL supplementation on the microbiota-gut-brain axis and the diet-induced obese phenotype in high fat (HF)-fed mice. Male C57/BL6 mice (n = 6/group; six weeks old) were counter-balanced into six weight-matched groups and fed either a low-fat (LF; 10% kcal as fat), HF (45% kcal as fat) or HF diet with 2′-FL (HF_2′-FL) at 1, 2, 5 and 10% (w/v) in drinking water for six weeks. General phenotypes (body weight, energy intake, fat and lean mass), cecal microbiome and metabolites, gut-brain signaling, intestinal permeability and inflammatory and lipid profiles were assessed. Only 10% 2′-FL, but not 1, 2 or 5%, decreased HF diet-induced increases in energy intake, fat mass and body weight gain. A supplementation of 10% 2′-FL changed the composition of cecal microbiota and metabolites compared to LF- and HF-fed mice with an increase in Parabacteroides abundance and lactate and pyruvate, respectively, whose metabolic effects corresponded to our study findings. In particular, 10% 2′-FL significantly reversed the HF diet-induced impairment of cholecystokinin-induced inhibition of food intake. Gene expressions of interleukin (IL)-1β, IL-6, and macrophage chemoattractant protein-1 in the cecum were significantly downregulated by 10% 2′-FL compared to the HF group. Furthermore, 10% 2′-FL suppressed HF diet-induced upregulation of hepatic peroxisome proliferator-activated receptor gamma, a transcription factor for adipogenesis, at the gene level. In conclusion, 10% 2′-FL led to compositional changes in gut microbiota and metabolites associated with improvements in metabolic profiles and gut-brain signaling in HF-fed mice. These findings support the use of 2′-FL for modulating the hyperphagic response to HF diets and improving the microbiota-gut-brain axis.

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