Article

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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    • "An equally important point is that the interaction between redox and immunological molecules regulate the gender cytokine immunological homeostasis in the control of inflammation. A key involvement of the interactions between the redox and the immune system in the inflammation and ageing process is concretely underlined by the correlation between the redox state, the functioning of the immune cells and the individual longevity2021222324. Therefore, relevant in this regard is that CD30, a membrane receptor (R) of the immunological cells, is the specific receptor of Thioredoxin1 (Trx1) on the immune cells[25](T and B cells, monocytes, dendritic cells, NK, eosinophils and granulocytes). "

    Full-text · Article · Jan 2016
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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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    Full-text · Article · Jan 2015 · Cytokine
    • "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.
    No preview · Article · Jan 2015 · Ageing Research Reviews
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