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Nutrition, Immunity, and Neurological Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutritional Immunology".

Deadline for manuscript submissions: closed (15 January 2022) | Viewed by 8544

Special Issue Editor

Molecular Medicine, IRCCS Stella Maris Foundation, Pisa, Italy
Interests: nutrition; neurogenetics; inflammation

Special Issue Information

Dear Colleagues,

There is an increase in susceptibility to chronic and debilitating diseases with aging, and the extent of severe neurodegenerative conditions has been increasingly rapidly in the early years of the 21st century. The reason for the underlying neuronal degeneration and normal aging of the brain remains elusive, and there is a growing emphasis on mechanisms related to inflammation, altered immune response, and genetic and dysfunctional cellular mechanisms such as autophagy and oxidative stress. Aging has proved to be modifiable, and so it could be for neurodegenerative conditions. By intervening in biological systems such as nutrient sensing, cellular senescence, the systemic environment, and the gut microbiome, phenotypes of neuronal death could be slowed sufficiently to mitigate age-related functional decline. These interventions have also been shown to delay the onset of chronic diseases including cancer, cardiovascular disease, and neurodegeneration in animal models. We believe that the time is ripe to focus on to how nutrients and nutraceutical compounds can modulate the processes underlying age-related conditions and inflammatory response in immune disorders. Thus, we put forward the idea to collect a series of high-standard manuscripts that fit the objectives and the topics of this Special Issue and raise awareness among colleagues about how nutrients can limit or delay neuronal cell death and impact the inflammatory response and immunological status in human diseases. We also believe that more research studies are necessary in order to determine the underlying mechanisms of how these essential nutrients work in the prevention of cognitive decline and cell death. Therefore, both clinical and basic research will be considered in this Special Issue.

Dr. Filippo M. Santorelli
Guest Editor

Manuscript Submission Information

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Keywords

  • Inflammation
  • Diet
  • Nutraceutics
  • Neurodegeneration
  • Immune Response

Published Papers (3 papers)

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Research

18 pages, 3621 KiB  
Article
β-Glucans as Dietary Supplement to Improve Locomotion and Mitochondrial Respiration in a Model of Duchenne Muscular Dystrophy
by Letizia Brogi, Maria Marchese, Alessandro Cellerino, Rosario Licitra, Valentina Naef, Serena Mero, Carlo Bibbiani and Baldassare Fronte
Nutrients 2021, 13(5), 1619; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051619 - 12 May 2021
Cited by 11 | Viewed by 2780
Abstract
Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular childhood disorder that causes progressive muscle weakness and degeneration. A lack of dystrophin in DMD leads to inflammatory response, autophagic dysregulation, and oxidative stress in skeletal muscle fibers that play a key role in [...] Read more.
Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular childhood disorder that causes progressive muscle weakness and degeneration. A lack of dystrophin in DMD leads to inflammatory response, autophagic dysregulation, and oxidative stress in skeletal muscle fibers that play a key role in the progression of the pathology. β-glucans can modulate immune function by modifying the phagocytic activity of immunocompetent cells, notably macrophages. Mitochondrial function is also involved in an important mechanism of the innate and adaptive immune responses, owing to high need for energy of immune cells. In the present study, the effects of 1,3-1,6 β-glucans on five-day-old non-dystrophic and dystrophic (sapje) zebrafish larvae were investigated. The effects of the sonication of β-glucans and the dechorionation of embryos were also evaluated. The results showed that the incidence of dystrophic phenotypes was reduced when dystrophic embryos were exposed to 2 and 4 mg L−1 of 1,3-1,6 β-glucans. Moreover, when the dystrophic larvae underwent 8 mg L−1 treatment, an improvement of the locomotor performances and mitochondrial respiration were observed. In conclusion, the observed results demonstrated that 1,3-1,6 β-glucans improve locomotor performances and mitochondrial function in dystrophic zebrafish. Therefore, for ameliorating their life quality, 1,3-1,6 β-glucans look like a promising diet supplement for DMD patients, even though further investigations are required. Full article
(This article belongs to the Special Issue Nutrition, Immunity, and Neurological Diseases)
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19 pages, 3085 KiB  
Article
Formyl Peptide Receptor (FPR)1 Modulation by Resveratrol in an LPS-Induced Neuroinflammatory Animal Model
by Rosa Calvello, Antonia Cianciulli, Chiara Porro, Piergianni Moda, Francesco De Nuccio, Giuseppe Nicolardi, Laura Giannotti, Maria Antonietta Panaro and Dario Domenico Lofrumento
Nutrients 2021, 13(5), 1418; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13051418 - 23 Apr 2021
Cited by 17 | Viewed by 2662
Abstract
Among therapeutic approaches that have been investigated, targeting of receptors implicated in managing neuroinflammation has been described. One such family of receptors comprises the formyl peptide receptors (FPRs) whose ligands could play a role in host defense. The murine FPR gene family includes [...] Read more.
Among therapeutic approaches that have been investigated, targeting of receptors implicated in managing neuroinflammation has been described. One such family of receptors comprises the formyl peptide receptors (FPRs) whose ligands could play a role in host defense. The murine FPR gene family includes at least six members while in humans there are only three. The two most important members are the Fpr1 and Fpr2. Fpr1encodes murine FPR1, which is considered the murine orthologue of human FPR. Resveratrol, a non-flavonoid polyphenol rich in red wine and grapes, apart from its beneficial health effects and anti-inflammatory properties, has been reported to reduce neuroinflammation in different neurodegenerative disease models. Resveratrol anti-inflammatory responses involve the activation of the protein deacetylase sirtuin 1 (SIRT1) gene. In this work we have investigated in an LPS-based murine model of neuroinflammation the role of FPR1, examining not only if this receptor undergoes a reduction of its expression during neuroinflammation, but also whether treatment with resveratrol was able to modulate its expression leading to an amelioration of neuroinflammatory picture in a murine model of neuroinflammation. Results of this work showed that FPR1 together with SIRT1 resulted upregulated by resveratrol treatment and that this increase is associated with an amelioration of the neuroinflammatory picture, as demonstrated by the induction of IL-10 and IL1-RA expression and the downregulation of proinflammatory mediators, such as TNF-α and IL-1β. The expression and the modulation of FPR1 by resveratrol may be evaluated in order to propose a novel anti-inflammatory and pro-resolving therapeutic approach for the reduction of the detrimental effects associated with neuro-inflammation based neurodegenerative diseases and also as a promising strategy to promote human health by a diet rich in antioxidative bioactive compounds. Full article
(This article belongs to the Special Issue Nutrition, Immunity, and Neurological Diseases)
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11 pages, 1214 KiB  
Article
Nutraceutical Screening in a Zebrafish Model of Muscular Dystrophy: Gingerol as a Possible Food Aid
by Rosario Licitra, Maria Marchese, Letizia Brogi, Baldassare Fronte, Letizia Pitto and Filippo M. Santorelli
Nutrients 2021, 13(3), 998; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13030998 - 19 Mar 2021
Cited by 11 | Viewed by 2336
Abstract
Duchenne muscular dystrophy (DMD), caused by mutations in the dystrophin gene, is an inherited neuromuscular disorder that causes loss of muscle mass and motor skills. In the era of genomic medicine, there is still no known cure for DMD. In clinical practice, there [...] Read more.
Duchenne muscular dystrophy (DMD), caused by mutations in the dystrophin gene, is an inherited neuromuscular disorder that causes loss of muscle mass and motor skills. In the era of genomic medicine, there is still no known cure for DMD. In clinical practice, there is a growing awareness of the possible importance of nutrition in neuromuscular diseases. This is mostly the result of patients’ or caregivers’ empirical reports of how active substances derived from food have led to improved muscle strength and, thus, better quality of life. In this report, we investigate several nutraceutical principles in the sapje strain of zebrafish, a validated model of DMD, in order to identify possible natural products that, if supplemented in the diet, might improve the quality of life of DMD patients. Gingerol, a constituent of fresh ginger, statistically increased the locomotion of mutant larvae and upregulated the expression of heme oxygenase 1, a target gene for therapy aimed at improving dystrophic symptoms. Although three other compounds showed a partial positive effect on locomotor and muscle structure phenotypes, our nutraceutical screening study lent preliminary support to the efficacy and safety only of gingerol. Gingerol could easily be proposed as a dietary supplement in DMD. Full article
(This article belongs to the Special Issue Nutrition, Immunity, and Neurological Diseases)
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