Oxidative stress, inflam-aging and immunosenescence

Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Journal of proteomics (Impact Factor: 3.89). 06/2011; 74(11):2313-23. DOI: 10.1016/j.jprot.2011.06.005
Source: PubMed

ABSTRACT Immunosenescence is characterized by a decreased ability of the immune system to respond to foreign antigens, as well as a decreased ability to maintain tolerance to self-antigens. This results in an increased susceptibility to infection and cancer and reduced responses to vaccination [1-5]. The mechanisms underlying immunosenescence comprise a series of cellular and molecular events involving alteration of several biochemical pathways and different cellular populations, and for the most part our understanding of these molecular mechanisms is still fragmentary. In this review we will focus on the process of senescence associated with oxidative stress, in particular how protein oxidation alters the functionality of immune cells and how oxidative stress contributes to a chronic inflammatory process often referred as inflamm-aging.

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Available from: Laura Santambrogio, Jan 20, 2014
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    • "The age-dependent increase in the serum levels of pro-inflammatory cytokines and a decrease in the levels of the anti-inflammatory cytokine demonstrated in this study are in agreement with previous studies [13] [27]. The mechanisms involved in the changes of circulating inflammatory mediators caused by aging are not fully understood, but changes related to immune senescence, such as gradual decline in protective immune response, deregulation of immune effector cells, and remodeling of cytokines and chemokine networks are proposed [28] [29]. "
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    ABSTRACT: a b s t r a c t The increase in the inflammatory process is one of the main factors that contribute to aging. The aim of this study was to investigate the effects of a diphenyl diselenide (PhSe) 2 -supplemented diet (1 p.p.m., 4 weeks) and swimming exercise (3% of body weight, 20 min per day, 4 weeks) on the serum levels of cytokines in Wistar rats of different ages. The results demonstrated an increase in the levels of pro-inflammatory cytokines (IL-1b, IL-6, TNFa and INFc) and a decrease in the levels of IL-10, an anti-inflammatory cytokine, with age. In middle-age rats, the swimming exercise and (PhSe) 2 -supplemented diet decreased serum levels of pro-inflammatory cytokines and increased the levels of IL-10. By contrast, in old rats the swimming exercise protocol increased the serum levels of pro-inflammatory cytokines and decreased the levels IL-10. Diet supplemented with (PhSe) 2 did not alter the serum levels of cytokines in old rats. Middle-age and old rats subjected to swimming exercise and supplemented with (PhSe) 2 in the diet had a decrease in the serum levels of pro-inflammatory cytokines and an increase in the levels of IL-10. This study demonstrated that swimming exercise and (PhSe) 2 -supplemented diet affect the serum levels of pro-and anti-inflammatory cytokines differently depending on the age of rats. (PhSe) 2 supplemented in the diet had an anti-inflammatory effect, similar to that of induced by swimming exercise, in middle-age rats and reversed the pro-inflammatory effects of swimming exercise in old rats.
    Cytokine 01/2015; 71(1). DOI:10.1016/j.cyto.2014.09.006 · 2.66 Impact Factor
    • "Despite the numerous studies on DAMPs in aging-associated pathologies, however, studies on DAMPs in healthy aging are scarce. It is known, however, that oxidative-stress, one of the main aging-related events, promotes inflammation in a TLRs and NLRP3 dependent manner (Cannizzo et al., 2011). Both TLR2 and TLR4 are stimulated by oxidized lipoproteins resulting in inflammation (Chávez-Sánchez et al., 2010), and NLRP3 is directly activated by the presence of sustained amounts of ROS (Chen and Nuñez , 2010). "
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    ABSTRACT: Accumulating evidence indicates that aging is associated with a chronic low-level inflammation, termed sterile-inflammation. Sterile-inflammation is a form of pathogen-free inflammation caused by mechanical trauma, ischemia, stress or environmental conditions such as ultra-violet radiation. These damage-related stimuli induce the secretion of molecular agents collectively termed danger-associated molecular patterns (DAMPs). DAMPs are recognized by virtue of specialized innate immune receptors, such as toll-like receptors (TLRs) and NOD-like receptor family, pyrin domain containing 3 (NLRP3). These receptors initiate signal transduction pathways, which typically drive inflammation in response to microbe-associated molecular patterns (MAMPs) and/or DAMPs. This review summarizes the current knowledge on DAMPs-mediated sterile-inflammation, its associated downstream signaling, and discusses the possibility that DAMPs activating TLRs or NLRP3 complex mediate sterile inflammation during aging and in aging-related pathologies. Copyright © 2015. Published by Elsevier B.V.
    Ageing Research Reviews 01/2015; DOI:10.1016/j.arr.2015.01.003 · 4.94 Impact Factor
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    • "Immunosenescence is accompanied by lymphocyte changes that include the accumulation of memory T cells, decreases in naïve lymphocytes and impaired effector T cell responses. In addition, a progression of chronic low-grade inflammation is observed during aging [3]. Elderly populations frequently suffer from an increase in disease and infections as the aged immune system responds inappropriately. "
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    ABSTRACT: The human immune system undergoes age-related changes that can lead to increased disease susceptibility. Using the baboon as a model for human immune system aging, we examined age-related changes in relative and absolute numbers of T cell subpopulations, cytomegalovirus (CMV) titer and markers of inflammation. In addition, the effect of gender, social status and peer group on lymphocyte subpopulations was determined. Relative and absolute numbers of total lymphocytes (CD3+), T helper cells (CD4+), and cytotoxic T cells (CD8+) increased with age. The proportion of naïve T cells (CD45RA+) decreased, while the total number of cells negative for the co-stimulatory receptor, CD28 (CD28-) increased in an age-dependent manner. Furthermore, CMV titers were negatively correlated with the number of naive CD4+ cells. IL-6 and cortisol concentration were also negatively associated with T cell subpopulations. Additionally, socially dominant baboons exhibited decreases in naïve CD4+ and CD8+ cells (by 65% and 52%, respectively) compared to subordinate animals. These results suggest that factors such as CMV exposure and inflammation may contribute to the age-related decline in immune health and indicate that factors like social status should be considered when studying immunosenescence in animal models.
    PLoS ONE 09/2014; 9(9):e107167. DOI:10.1371/journal.pone.0107167 · 3.23 Impact Factor
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