New Insights about Regulatory T Cells Distribution and Function with Exercise: The Role of Immunometabolism

2020 ◽  
Vol 26 (9) ◽  
pp. 979-990 ◽  
Author(s):  
Gilson P. Dorneles ◽  
Aline A.Z. dos Passos ◽  
Pedro R.T. Romão ◽  
Alessandra Peres
Keyword(s):  
T Cells ◽  
Chronic Diseases ◽  
Experimental Studies ◽  
Treg Cells ◽  
Metabolic Phenotype ◽  
Acid Oxidation ◽  
Low Grade ◽  
And Function ◽  
Low Grade Inflammation

A lack of physical activity is linked to the development of many chronic diseases through a chronic low-grade inflammation state. It is now well accepted that the immune system plays a central role in the development of several chronic diseases, including insulin resistance, type 2 diabetes, atherosclerosis, heart failure and certain types of cancer. Exercise elicits a strong anti-inflammatory response independently of weight loss and can be a useful non-pharmacologic strategy to counteract the low-grade inflammation. The CD4+CD25+CD127- FoxP3+ Regulatory T (Treg) cells are a unique subset of helper T-cells, which regulate immune response and establish self-tolerance through the secretion of immunoregulatory cytokines, such as IL-10 and TGF-β, and the suppression of the function and activity of many immune effector cells (including monocytes/macrophages, dendritic cells, CD4+ and CD8+ T cells, and Natural Killers). The metabolic phenotype of Tregs are regulated by the transcription factor Foxp3, providing flexibility in fuel choice, but a preference for higher fatty acid oxidation. In this review, we focus on the mechanisms by which exercise - both acute and chronic - exerts its antiinflammatory effects through Treg cells mobilization. Furthermore, we discuss the implications of immunometabolic changes during exercise for the modulation of Treg phenotype and its immunosuppressive function. This narrative review focuses on the current knowledge regarding the role of Treg cells in the context of acute and chronic exercise using data from observational and experimental studies. Emerging evidence suggests that the immunomodulatory effects of exercise are mediated by the ability of exercise to adjust and improve Tregs number and function.

scholarly journals Inflammatory Bowel Diseases and Sarcopenia: The Role of Inflammation and Gut Microbiota in the Development of Muscle Failure

2021 ◽  
Vol 12 ◽  
Author(s):  
Olga Maria Nardone ◽  
Roberto de Sire ◽  
Valentina Petito ◽  
Anna Testa ◽  
Guido Villani ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Adverse Outcomes ◽  
Low Grade ◽  
Increased Risk ◽  
Bowel Diseases ◽  
Inflammatory Bowel ◽  
And Function ◽  
Host Metabolism ◽  
Low Grade Inflammation

Sarcopenia represents a major health burden in industrialized country by reducing substantially the quality of life. Indeed, it is characterized by a progressive and generalized loss of muscle mass and function, leading to an increased risk of adverse outcomes and hospitalizations. Several factors are involved in the pathogenesis of sarcopenia, such as aging, inflammation, mitochondrial dysfunction, and insulin resistance. Recently, it has been reported that more than one third of inflammatory bowel disease (IBD) patients suffered from sarcopenia. Notably, the role of gut microbiota (GM) in developing muscle failure in IBD patient is a matter of increasing interest. It has been hypothesized that gut dysbiosis, that typically characterizes IBD, might alter the immune response and host metabolism, promoting a low-grade inflammation status able to up-regulate several molecular pathways related to sarcopenia. Therefore, we aim to describe the basis of IBD-related sarcopenia and provide the rationale for new potential therapeutic targets that may regulate the gut-muscle axis in IBD patients.

scholarly journals Endothelial Aldehyde Dehydrogenase 2 as a Target to Maintain Vascular Wellness and Function in Ageing

Biomedicines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 4 ◽  
Author(s):  
Ginevra Nannelli ◽  
Marina Ziche ◽  
Sandra Donnini ◽  
Lucia Morbidelli
Keyword(s):  
Aldehyde Dehydrogenase ◽  
Vascular Function ◽  
Vascular Dysfunction ◽  
Low Grade ◽  
Loss Of Function ◽  
Aldehyde Dehydrogenase 2 ◽  
Main Determinants ◽  
And Function ◽  
Low Grade Inflammation

Endothelial cells are the main determinants of vascular function, since their dysfunction in response to a series of cardiovascular risk factors is responsible for disease progression and further consequences. Endothelial dysfunction, if not resolved, further aggravates the oxidative status and vessel wall inflammation, thus igniting a vicious cycle. We have furthermore to consider the physiological manifestation of vascular dysfunction and chronic low-grade inflammation during ageing, also known as inflammageing. Based on these considerations, knowledge of the molecular mechanism(s) responsible for endothelial loss-of-function can be pivotal to identify novel targets of intervention with the aim of maintaining endothelial wellness and vessel trophism and function. In this review we have examined the role of the detoxifying enzyme aldehyde dehydrogenase 2 (ALDH2) in the maintenance of endothelial function. Its impairment indeed is associated with oxidative stress and ageing, and in the development of atherosclerosis and neurodegenerative diseases. Strategies to improve its expression and activity may be beneficial in these largely diffused disorders.

CD8 Treg-Mediated Suppression of Naive CD4+ T Cell Differentiation into Follicular Helper T Cells

2021 ◽  
pp. 1-11
Author(s):  
Taissa M. Kasahara ◽  
Sudhir Gupta
Keyword(s):  
T Cells ◽  
Cell Differentiation ◽  
T Cell ◽  
Inflammatory Responses ◽  
Treg Cells ◽  
Follicular Helper ◽  
And Function ◽  
Proliferation In Vitro

<b><i>Background:</i></b> The regulatory CD8<sup>+</sup> T (CD8<sup>+</sup> Treg) cells play an important role in immune tolerance and have been implicated in several human autoimmune diseases. In this context, follicular helper T (T<sub>FH</sub>) cells contribute by controlling the antibody production. In mice, CD8<sup>+</sup> Treg cells control the number and function of T<sub>FH</sub> cells however the role of human CD8<sup>+</sup> Treg cells on the differentiation of naive CD4<sup>+</sup> T cells into T<sub>FH</sub> cells has not been studied. <b><i>Objectives:</i></b> Here, we evaluated the ability of human CD183<sup>+</sup> CD8<sup>+</sup> Treg cells to suppress T<sub>FH</sub> cell differentiation in vitro. <b><i>Methods:</i></b> Activated CD183<sup>+</sup>CCR7<sup>+</sup>CD45RA<sup>−</sup>CD8<sup>+</sup> Treg and CD183<sup>+</sup>CD25<sup>high</sup>ICOS<sup>+</sup>CD8<sup>+</sup> Treg cells were sorted and cocultured with naïve CD4<sup>+</sup> T cells under T<sub>FH</sub> differentiation condition. The differentiation of T<sub>FH</sub> cells was evaluated by flow cytometry. <b><i>Results:</i></b> Our results showed that activated CD183<sup>+</sup>CD8<sup>+</sup> Treg cells upregulated the expression of Forkhead box P3 transcription factor, inducible T-cell co-stimulator (ICOS), and CD25 compared to CD183<sup>−</sup>CD8<sup>+</sup> T cells. The CD183<sup>+</sup>CD25<sup>high</sup>ICOS<sup>+</sup>CD8<sup>+</sup> Treg cells suppressed T<sub>FH</sub> cell differentiation and CD4<sup>+</sup> T cell proliferation in vitro which was not observed when CD183<sup>+</sup>CCR7<sup>+</sup>CD45RA<sup>−</sup>CD8<sup>+</sup> Treg were cocultured with naïve CD4<sup>+</sup> T cells under T<sub>FH</sub> cell differentiation condition. <b><i>Conclusion:</i></b> These results suggest that CD25<sup>high</sup>ICOS<sup>+</sup>CD183<sup>+</sup>CD8<sup>+</sup> Treg cells may regulate autoimmune and inflammatory responses mediated by T<sub>FH</sub> cells.

scholarly journals Nutrients, Nutraceuticals and Xenobiotics Affecting Renal Health

2018 ◽  
Author(s):  
Carmela Cosola ◽  
Alice Sabatino ◽  
Ighli di Bari ◽  
Enrico Fiaccadori ◽  
Loreto Gesualdo
Keyword(s):  
Risk Factors ◽  
Renal Damage ◽  
Developed Countries ◽  
Steviol Glycosides ◽  
Low Grade ◽  
Salt Restriction ◽  
Dietary Components ◽  
And Function ◽  
Low Grade Inflammation

Chronic kidney disease (CKD) affects worldwide 8-16% of the population. In developed countries, the most important risk factors for CKD are diabetes, hypertension and obesity, calling into question the importance of educating and acting on lifestyles and nutrition. A balanced nutrition and supplementation can indeed support the maintenance of a general health status, including preservation of renal function, and help to manage and curb the main risk factors for renal damage. While the concepts of protein and salt restriction in nephrology are historically acknowledged, the role of some nutrients on renal health and the importance of nutrition as a preventative measure for renal care are less known. In this review, we provide an overview of the demonstrated and potential actions of some selected nutrients, nutraceuticals and xenobiotics on renal health and function. The effects on kidney of fibres, proteins, fatty acids, curcumin, steviol glycosides, green tea, coffee, nitrates, nitrites, and alcohol, both direct and indirect, in CKD and non-CKD condition, are reviewed here. In a view of a functional and personalized nutrition, understanding the renal and systemic effects of dietary components is essential since many chronic conditions and CKD are related to systemic dysfunctions such as chronic low-grade inflammation.

scholarly journals Mitochondrial (Dys) Function in Inflammaging: Do MitomiRs Influence the Energetic, Oxidative, and Inflammatory Status of Senescent Cells?

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Angelica Giuliani ◽  
Francesco Prattichizzo ◽  
Luigina Micolucci ◽  
Antonio Ceriello ◽  
Antonio Domenico Procopio ◽  
...  
Keyword(s):  
Mitochondrial Gene ◽  
Low Grade ◽  
Master Regulators ◽  
Inflammatory Status ◽  
Age Related ◽  
Secretory Phenotype ◽  
And Function ◽  
Low Grade Inflammation ◽  
Proinflammatory Factors

A relevant feature of aging is chronic low-grade inflammation, termed inflammaging, a key process promoting the development of all major age-related diseases. Senescent cells can acquire the senescence-associated (SA) secretory phenotype (SASP), characterized by the secretion of proinflammatory factors fuelling inflammaging. Cellular senescence is also accompanied by a deep reshaping of microRNA expression and by the modulation of mitochondria activity, both master regulators of the SASP. Here, we synthesize novel findings regarding the role of mitochondria in the SASP and in the inflammaging process and propose a network linking nuclear-encoded SA-miRNAs to mitochondrial gene regulation and function in aging cells. In this conceptual structure, SA-miRNAs can translocate to mitochondria (SA-mitomiRs) and may affect the energetic, oxidative, and inflammatory status of senescent cells. We discuss the potential role of several of SA-mitomiRs (i.e., let-7b, miR-1, miR-130a-3p, miR-133a, miR-146a-5p, miR-181c-5p, and miR-378-5p), using miR-146a as a proof-of-principle model. Finally, we propose a comprehensive, metabolic, and epigenetic view of the senescence process, in order to amplify the range of possible approaches to target inflammaging, with the ultimate goal of decelerating the aging rate, postponing or blunting the development of age-related diseases.

The Role of Epicardial Adipose Tissue Lymphocytes in Low-Grade Inflammation and Coronary Artery Disease

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 469-P
Author(s):  
MILOS MRAZ ◽  
ANNA CINKAJZLOVA ◽  
ZDENA LACINOVÁ ◽  
JANA KLOUCKOVA ◽  
HELENA KRATOCHVILOVA ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Epicardial Adipose Tissue ◽  
Low Grade ◽  
Artery Disease ◽  
Low Grade Inflammation

scholarly journals Consumption of Select Dietary Emulsifiers Exacerbates the Development of Spontaneous Intestinal Adenoma

2021 ◽  
Vol 22 (5) ◽  
pp. 2602
Author(s):  
Emilie Viennois ◽  
Benoit Chassaing
Keyword(s):  
Intestinal Inflammation ◽  
Tumor Development ◽  
Low Grade ◽  
Gastrointestinal Cancers ◽  
Cancer Initiation ◽  
And Function ◽  
The Impact ◽  
Chronic Intestinal Inflammation ◽  
Low Grade Inflammation ◽  
Intestinal Adenoma

Inflammation is a well-characterized critical driver of gastrointestinal cancers. Previous findings have shown that intestinal low-grade inflammation can be promoted by the consumption of select dietary emulsifiers, ubiquitous component of processed foods which alter the composition and function of the gut microbiota. Using a model of colitis-associated cancer, we previously reported that consumption of the dietary emulsifiers carboxymethylcellulose or polysorbate-80 exacerbated colonic tumor development. Here, we investigate the impact of dietary emulsifiers consumption on cancer initiation and progression in a genetical model of intestinal adenomas. In APCmin mice, we observed that dietary emulsifiers consumption enhanced small-intestine tumor development in a way that appeared to be independent of chronic intestinal inflammation but rather associated with emulsifiers’ impact on the proliferative status of the intestinal epithelium as well as on intestinal microbiota composition in both male and female mice. Overall, our findings further support the hypothesis that emulsifier consumption may be a new modifiable risk factor for colorectal cancer (CRC) and that alterations in host–microbiota interactions can favor gastrointestinal carcinogenesis in individuals with a genetical predisposition to such disorders.

scholarly journals Trichostatin A Promotes the Generation and Suppressive Functions of Regulatory T Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Cristian Doñas ◽  
Macarena Fritz ◽  
Valeria Manríquez ◽  
Gabriela Tejón ◽  
María Rosa Bono ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Trichostatin A ◽  
Gene Promoter ◽  
Treg Cells ◽  
Specific Subset ◽  
Global Increase ◽  
And Function ◽  
H3 Acetylation

Regulatory T cells are a specific subset of lymphocytes that suppress immune responses and play a crucial role in the maintenance of self-tolerance. They can be generated in the thymus as well as in the periphery through differentiation of naïve CD4+T cells. The forkhead box P3 transcription factor (Foxp3) is a crucial molecule regulating the generation and function of Tregs. Here we show that thefoxp3gene promoter becomes hyperacetylated inin vitrodifferentiated Tregs compared to naïve CD4+T cells. We also show that the histone deacetylase inhibitor TSA stimulated thein vitrodifferentiation of naïve CD4+T cells into Tregs and that this induction was accompanied by a global increase in histone H3 acetylation. Importantly, we also demonstrated that Tregs generated in the presence of TSA have phenotypical and functional differences from the Tregs generated in the absence of TSA. Thus, TSA-generated Tregs showed increased suppressive activities, which could potentially be explained by a mechanism involving the ectonucleotidases CD39 and CD73. Our data show that TSA could potentially be used to enhance the differentiation and suppressive function of CD4+Foxp3+Treg cells.

scholarly journals Centromere Protein B Null Mice are Mitotically and Meiotically Normal but Have Lower Body and Testis Weights

1998 ◽  
Vol 141 (2) ◽  
pp. 309-319 ◽  
Author(s):  
Damien F. Hudson ◽  
Kerry J. Fowler ◽  
Elizabeth Earle ◽  
Richard Saffery ◽  
Paul Kalitsis ◽  
...  
Keyword(s):  
Cell Cycle Progression ◽  
Mammalian Species ◽  
Experimental Studies ◽  
Conflicting Evidence ◽  
Body Weights ◽  
Reduced Rate ◽  
And Function ◽  
Centromere Assembly ◽  
Mitosis And Meiosis

CENP-B is a constitutive centromere DNA-binding protein that is conserved in a number of mammalian species and in yeast. Despite this conservation, earlier cytological and indirect experimental studies have provided conflicting evidence concerning the role of this protein in mitosis. The requirement of this protein in meiosis has also not previously been described. To resolve these uncertainties, we used targeted disruption of the Cenpb gene in mouse to study the functional significance of this protein in mitosis and meiosis. Male and female Cenpb null mice have normal body weights at birth and at weaning, but these subsequently lag behind those of the heterozygous and wild-type animals. The weight and sperm content of the testes of Cenpb null mice are also significantly decreased. Otherwise, the animals appear developmentally and reproductively normal. Cytogenetic fluorescence-activated cell sorting and histological analyses of somatic and germline tissues revealed no abnormality. These results indicate that Cenpb is not essential for mitosis or meiosis, although the observed weight reduction raises the possibility that Cenpb deficiency may subtly affect some aspects of centromere assembly and function, and result in reduced rate of cell cycle progression, efficiency of microtubule capture, and/or chromosome movement. A model for a functional redundancy of this protein is presented.

scholarly journals Adipose tissue inflammation and metabolic dysfunction: a clinical perspective

2013 ◽  
Vol 15 (1) ◽  
Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Low Grade ◽  
Metabolic Dysfunction ◽  
Adipose Tissue Inflammation ◽  
Tissue Inflammation ◽  
Proinflammatory Mediators ◽  
Low Grade Inflammation

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).

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