scholarly journals Nutritional Modulation of Immune and Central Nervous System Homeostasis: The Role of Diet in Development of Neuroinflammation and Neurological Disease

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1076 ◽  
Author(s):  
José Antonio Estrada ◽  
Irazú Contreras
Keyword(s):  
Immune System ◽  
Dietary Patterns ◽  
Neurological Disease ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Treg Cells ◽  
Signaling Molecules ◽  
Metabolic Alterations ◽  
Microbiome Composition

The gut-microbiome-brain axis is now recognized as an essential part in the regulation of systemic metabolism and homeostasis. Accumulating evidence has demonstrated that dietary patterns can influence the development of metabolic alterations and inflammation through the effects of nutrients on a multitude of variables, including microbiome composition, release of microbial products, gastrointestinal signaling molecules, and neurotransmitters. These signaling molecules are, in turn, implicated in the regulation of the immune system, either promoting or inhibiting the production of pro-inflammatory cytokines and the expansion of specific leukocyte subpopulations, such as Th17 and Treg cells, which are relevant in the development of neuroinflammatory and neurodegenerative conditions. Metabolic diseases, like obesity and type 2 diabetes mellitus, are related to inadequate dietary patterns and promote variations in the aforementioned signaling pathways in patients with these conditions, which have been linked to alterations in neurological functions and mental health. Thus, maintenance of adequate dietary patterns should be an essential component of any strategy aiming to prevent neurological pathologies derived from systemic metabolic alterations. The present review summarizes current knowledge on the role of nutrition in the modulation of the immune system and its impact in the development of neuroinflammation and neurological disease.

scholarly journals Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?

2021 ◽  
Vol 12 ◽  
Author(s):  
Chiel van Geffen ◽  
Astrid Deißler ◽  
Markus Quante ◽  
Harald Renz ◽  
Dominik Hartl ◽  
...  
Keyword(s):  
Immune System ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Immune Responses ◽  
Immune Cells ◽  
Current Knowledge ◽  
Suppressor Cells ◽  
Interstitial Lung Diseases ◽  
Stromal Stem Cells

The immune system is receiving increasing attention for interstitial lung diseases, as knowledge on its role in fibrosis development and response to therapies is expanding. Uncontrolled immune responses and unbalanced injury-inflammation-repair processes drive the initiation and progression of idiopathic pulmonary fibrosis. The regulatory immune system plays important roles in controlling pathogenic immune responses, regulating inflammation and modulating the transition of inflammation to fibrosis. This review aims to summarize and critically discuss the current knowledge on the potential role of regulatory immune cells, including mesenchymal stromal/stem cells, regulatory T cells, regulatory B cells, macrophages, dendritic cells and myeloid-derived suppressor cells in idiopathic pulmonary fibrosis. Furthermore, we review the emerging role of regulatory immune cells in anti-fibrotic therapy and lung transplantation. A comprehensive understanding of immune regulation could pave the way towards new therapeutic or preventive approaches in idiopathic pulmonary fibrosis.

scholarly journals Balance between Regulatory T and Th17 Cells in Systemic Lupus Erythematosus: The Old and the New

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Alessia Alunno ◽  
Elena Bartoloni ◽  
Onelia Bistoni ◽  
Giuseppe Nocentini ◽  
Simona Ronchetti ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Lymphocytes ◽  
Lupus Erythematosus ◽  
Th17 Cells ◽  
Current Knowledge ◽  
Treg Cells ◽  
T Helper ◽  
Systemic Lupus ◽  
Target Organs

Pathogenic mechanisms underlying the development of systemic lupus erythematosus (SLE) are very complex and not yet entirely clarified. However, the pivotal role of T lymphocytes in the induction and perpetuation of aberrant immune response is well established. Among T cells, IL-17 producing T helper (Th17) cells and regulatory T (Treg) cells represent an intriguing issue to be addressed in SLE pathogenesis, since an imbalance between the two subsets has been observed in the course of the disease. Treg cells appear to be impaired and therefore unable to counteract autoreactive T lymphocytes. Conversely, Th17 cells accumulate in target organs contributing to local IL-17 production and eventually tissue damage. In this setting, targeting Treg/Th17 balance for therapeutic purposes may represent an intriguing and useful tool for SLE treatment in the next future. In this paper, the current knowledge about Treg and Th17 cells interplay in SLE will be discussed.

scholarly journals A tobozmirigy-csecsemőmirigy rendszer szerepe az autoimmunitás, öregedés és élettartam szabályozásában

2016 ◽  
Vol 157 (27) ◽  
pp. 1065-1070 ◽  
Author(s):  
György Csaba
Keyword(s):  
Immune System ◽  
Pineal Gland ◽  
Mass Function ◽  
Treg Cells ◽  
Autoimmune Process ◽  
Wasting Disease ◽  
Pacemaker Function ◽  
Autoreactive Cells ◽  
End Of Puberty

Thymus is an immunoendocrine organ, the hormones of which mainly influence its own lymphatic elements. It has a central role in the immune system, the neonatal removal causes the collapse of immune system and the whole organism. The thymic nurse cells select the bone marrow originated lymphocytes and destroy the autoreactive ones, while thymus originated Treg cells suppress the autoreactive cells in the periphery. The involution of the organ starts after birth, however, this truly happens in the end of puberty only, as before this it is overcompensated by developmental processes. From the end of adolescence the involution allows the life, proliferation and enhanced functioning of some autoreactive cells, which gradually wear down the cells and intercellular materials, causing the aging. The enhanced and mass function of autoreactive cells lead to the autoimmune diseases and natural death. This means that the involution of thymus is not a part of the organismic involution, but an originator of it, which is manifested in the lifespan-pacemaker function. In this case aging can be comprehended as a thymus-commanded slow autoimmune process. The neonatal removal of pineal gland leads to the complete destruction of the thymus and the crashing down of the immune system, as well as to wasting disease. The involution of the pineal and thymus runs parallel, because the two organs form a functional unit. It is probable that the pineal gland is responsible for the involution of thymus and also regulates its lifespan determining role. The data reviewed do not prove the exclusive role of pineal-thymus system in the regulation of aging and lifespan, however, calls attention to the suitability of solving this problem alone. Orv. Hetil., 2016, 157(27), 1065–1070.

scholarly journals Intracellular and Extracellular Roles of Granzyme K

2021 ◽  
Vol 12 ◽  
Author(s):  
Annemieke C. Bouwman ◽  
Kim R. van Daalen ◽  
Sandra Crnko ◽  
Toine ten Broeke ◽  
Niels Bovenschen
Keyword(s):  
Immune System ◽  
Therapeutic Target ◽  
Serine Proteases ◽  
Bacterial Infections ◽  
Thermal Injury ◽  
Current Knowledge ◽  
Endothelial Activation ◽  
Potential Therapeutic Target ◽  
Cytotoxic Cells

Granzymes are a family of serine proteases stored in granules inside cytotoxic cells of the immune system. Granzyme K (GrK) has been only limitedly characterized and knowledge on its molecular functions is emerging. Traditionally GrK is described as a granule-secreted, pro-apoptotic serine protease. However, accumulating evidence is redefining the functions of GrK by the discovery of novel intracellular (e.g. cytotoxicity, inhibition of viral replication) and extracellular roles (e.g. endothelial activation and modulation of a pro-inflammatory immune cytokine response). Moreover, elevated GrK levels are associated with disease, including viral and bacterial infections, airway inflammation and thermal injury. This review aims to summarize and discuss the current knowledge of i) intracellular and extracellular GrK activity, ii) cytotoxic and non-cytotoxic GrK functioning, iii) the role of GrK in disease, and iv) GrK as a potential therapeutic target.

scholarly journals A new insight into tumor immune-evasion: Crosstalk between cancer stem cells and T regulatory cells

2020 ◽  
Author(s):  
Abhishek Dutta ◽  
Debomita Sengupta ◽  
Swastika Paul ◽  
Sourio Chakraborty ◽  
Tanya Das
Keyword(s):  
Stem Cells ◽  
T Cells ◽  
Immune System ◽  
Cancer Stem Cells ◽  
Treg Cell ◽  
Significant Role ◽  
Treg Cells ◽  
Cell Generation ◽  
Naïve T Cells

Cancer development is initiated, sustained, and aggravated by a rare population of cells, termed cancer stem cells (CSCs). Although CSCs are considered as a promising source of cells to orchestrate the immune system to work in favour of tumor, the detailed mechanisms underlying their immunomodulatory effects remain elusive. Recent reports indicate the contribution of exosomes, secreted from various cells, as mediators of cell-to-cell communication especially within the tumor microenvironment. We aimed at exploring the role of CSC-derived exosomes (CDEs) in reprogramming the host immune system by generating functional T-regulatory (Treg) cells, and at delineating the underlying mechanisms. Our results showed that CDEs play a significant role in generating CD4 + CD25 + FoxP3 + Treg cells from naive T-cells. A search for the underlying mechanism revealed the presence of FoxP3 protein in CDEs which was found to be transferred to the naïve T-cells. Exosomes from FoxP3-ablated CSCs failed to augment immuno-suppressive Treg cell generation confirming the significant role of the transported protein. In order to understand the contribution of CDE-FoxP3 in maintaining a heritably stable population of Treg cell we checked for the binding of CDE-FoxP3 on conserved non-coding sequence 2 (CNS2) region of FoxP3 promoter in T-naïve cells and found CDE-FoxP3 is indeed recruited to the CNS2 region generating stable and functionally suppressive Treg cells. These results raise the possibility that CSCs provide the initial trigger for immunosuppressive Treg cell generation and thus, breaching the deadly-liaison between them might be a promising strategy in breast cancer therapy.

scholarly journals Neutrophils—From Bone Marrow to First-Line Defense of the Innate Immune System

2021 ◽  
Vol 12 ◽  
Author(s):  
Richard Felix Kraus ◽  
Michael Andreas Gruber
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Current Knowledge ◽  
Immune Defense ◽  
Innate Immune ◽  
Human Organism ◽  
Polymorphonuclear Cells ◽  
Target Tissue ◽  
First Line

Neutrophils (polymorphonuclear cells; PMNs) form a first line of defense against pathogens and are therefore an important component of the innate immune response. As a result of poorly controlled activation, however, PMNs can also mediate tissue damage in numerous diseases, often by increasing tissue inflammation and injury. According to current knowledge, PMNs are not only part of the pathogenesis of infectious and autoimmune diseases but also of conditions with disturbed tissue homeostasis such as trauma and shock. Scientific advances in the past two decades have changed the role of neutrophils from that of solely immune defense cells to cells that are responsible for the general integrity of the body, even in the absence of pathogens. To better understand PMN function in the human organism, our review outlines the role of PMNs within the innate immune system. This review provides an overview of the migration of PMNs from the vascular compartment to the target tissue as well as their chemotactic processes and illuminates crucial neutrophil immune properties at the site of the lesion. The review is focused on the formation of chemotactic gradients in interaction with the extracellular matrix (ECM) and the influence of the ECM on PMN function. In addition, our review summarizes current knowledge about the phenomenon of bidirectional and reverse PMN migration, neutrophil microtubules, and the microtubule organizing center in PMN migration. As a conclusive feature, we review and discuss new findings about neutrophil behavior in cancer environment and tumor tissue.

scholarly journals Short chain fatty acids (SCFA), the products of gut bacteria metabolism and their role in the host

2018 ◽  
Vol 72 ◽  
pp. 131-142 ◽  
Author(s):  
Aleksandra Czajkowska ◽  
Bogumiła Szponar
Keyword(s):  
Fatty Acids ◽  
Immune System ◽  
Short Chain Fatty Acids ◽  
Gastrointestinal Diseases ◽  
Bacterial Consortium ◽  
Treg Cells ◽  
Short Chain ◽  
Microbiome Composition ◽  
Promising Tool ◽  
Chain Fatty Acids

Gut bacterial consortium is essential for the homeostasis of the immune system in mammals. A significant role in maintaining this balance play short-chain fatty acids (SCFA), bacterial metabolites resulting from fermentation of dietary oligosaccharides. The most significant are butyric, propionic and acetic acids present in the microbiome in a specified mole ratio, but these proportions may change due to diet, age, diseases, and other factors. SCFA are the type of messengers between microbiota and immune system. They are responsible for maintaining the balance in the pro- and anti-inflammatory reaction through the set of free fatty acid receptors (GPR). Short chain fatty acids may induce regulatory T-cells (Treg) by an bakteinhibition of histone deacetylase enzyme; the biggest inhibitory potential has butyric acid, causing proliferation and an increase of the functional capabilities of Treg cells. Manipulation of the gut microbiome composition and SCFA level constitutes a promising tool supporting treatment of chronic gastrointestinal diseases associated with an inflammation or caused by dysbiosis due to intensive use of antibiotics.

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.

scholarly journals Role of Dietary Lipids in Modulating Inflammation through the Gut Microbiota

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 117 ◽  
Author(s):  
Paul J. Wisniewski ◽  
Robert A. Dowden ◽  
Sara C. Campbell
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Current Knowledge ◽  
Endocannabinoid System ◽  
Dietary Lipids ◽  
Taxonomic Resolution ◽  
Low Grade ◽  
Energy Regulation ◽  
Microbial Dysbiosis

Inflammation and its resolution is a tenuous balance that is under constant contest. Though several regulatory mechanisms are employed to maintain homeostasis, disruptions in the regulation of inflammation can lead to detrimental effects for the host. Of note, the gut and microbial dysbiosis are implicated in the pathology of systemic chronic low-grade inflammation which has been linked to several metabolic diseases. What remains to be described is the extent to which dietary fat and concomitant changes in the gut microbiota contribute to, or arise from, the onset of metabolic disorders. The present review will highlight the role of microorganisms in host energy regulation and several mechanisms that contribute to inflammatory pathways. This review will also discuss the immunomodulatory effects of the endocannabinoid system and its link with the gut microbiota. Finally, a brief discussion arguing for improved taxonomic resolution (at the species and strain level) is needed to deepen our current knowledge of the microbiota and host inflammatory state.

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