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Antioxidants
Special Issues
Redox Regulation of the Innate Immunity and Aging
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Redox Regulation of the Innate Immunity and Aging

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3798

Special Issue Editor

Dr. Svetlana N. Radyuk

E-Mail Website
Guest Editor
Department of Biological Sciences, Southern Methodist University, Dallas, TX, USA
Interests: redox; immunity; aging; age-related diseases; peroxiredoxins; stress response signaling

Special Issue Information

Dear Colleagues,

At present, numerous data have been accumulated on the role of the redox in the regulation of immunity. Redox is involved in the modulation of the functions of adaptive and innate immune cells, and also mediates their interaction. Redox sensitive components are found in signaling pathways that regulate the immune response. The activation of the immune response occurs in parallel with the release of reactive oxygen species and reactive nitrogen species, which in turn act as triggers, mediators or modulators of pathways involved in immune regulation.

Immune responses tend to be deregulated during aging. While the efficiency of adaptive immunity declines, innate immunity exhibits a shift toward an excessive response and inflammation. Recently, there has been increasing interest in the hyperactive immune response in the absence of infection, or so-called sterile inflammation—a phenomenon with a potential age-related component. Among the inflammatory triggers are reactive oxygen species, changes in redox, and redox-related damages. Changes in cellular redox and a shift towards a pro-oxidant state are also associated with aging, and disbalanced redox is considered a major contributor to aging and premature senescence.

This Special Issue welcomes original research papers and review articles related to the study of the relationship between immunity and aging and their control by redox-sensitive components. Submissions can be devoted to the following issues:

  • Identification of changes in the immune system leading to increase in the chronic pro-inflammatory state;
  • Identification of new redox-sensitive components of the immune signaling pathways;
  • Identification of factors that lead to chronic inflammation in the aging process;
  • Defining the mechanisms that govern the inter-relationship between innate immunity and aging;
  • Epigenetic regulation of the immune pathways and identification of the redox-sensitive epigenetic modifications involved in the regulation of aging and age-related immune function;
  • Redox regulation of mucosal immunity;
  • The role of small molecules/compounds, including low-molecular-weight thiols and biological gases, in modulating the immune response during aging;
  • Inflammaging.

Dr. Svetlana N. Radyuk
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • redox
  • aging
  • immunity
  • epigenetics
  • inflammation
  • inflammaging

Published Papers (2 papers)

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14 pages, 680 KiB  
Article
Sarcopenia Is Associated with Changes in Circulating Markers of Antioxidant/Oxidant Balance and Innate Immune Response
by Francesco Bellanti, Aurelio Lo Buglio, Stefano Quiete, Michał Dobrakowski, Aleksandra Kasperczyk, Sławomir Kasperczyk and Gianluigi Vendemiale
Antioxidants 2023, 12(11), 1992; https://doi.org/10.3390/antiox12111992 - 11 Nov 2023
Viewed by 941
Abstract
(1) Background: The involvement of redox balance alterations and innate immunity is suggested to play a key role in the pathogenesis of sarcopenia. This investigation aimed to define and relate modifications in circulating markers of redox homeostasis and the innate immune response in [...] Read more.
(1) Background: The involvement of redox balance alterations and innate immunity is suggested to play a key role in the pathogenesis of sarcopenia. This investigation aimed to define and relate modifications in circulating markers of redox homeostasis and the innate immune response in human sarcopenia. (2) Methods: A total of 32 subjects aged >65 years old and affected by sarcopenia according to the second “European Working Group on sarcopenia in older people” guidelines were compared with 40 non-sarcopenic age-matched controls. To assess systemic redox homeostasis, reduced (GSH) and oxidized (GSSG) blood glutathione and plasma malondialdehyde (MDA)– and 4-hydroxy-2,3-nonenal (HNE)–protein adducts were measured. Immune cells and circulating interleukins were determined to compare the innate immune response between both groups. (3) Results: Impaired redox balance in sarcopenic patients, characterized by a high blood GSSG/GSH ratio and plasma MDA/HNE–protein adducts, was sustained by reduced antioxidants in peripheral blood mononuclear cells. Furthermore, sarcopenic patients showed higher neutrophil-to-lymphocyte ratios and interleukin (IL)-4, IL-6, IL-10, and tumor necrosis factor (TNF) with respect to non-sarcopenic patients. Linear regression analysis resulted in a strong association between redox balance and immune response markers in the sarcopenic group. (4) Conclusions: These results support the interplay between redox homeostasis alteration and disruption of the innate immune response in the pathogenesis of sarcopenia. Full article
(This article belongs to the Special Issue Redox Regulation of the Innate Immunity and Aging)
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14 pages, 1999 KiB  
Article
Glycolysis and the Pentose Phosphate Pathway Promote LPS-Induced NOX2 Oxidase- and IFN-β-Dependent Inflammation in Macrophages
by Jonathan R. Erlich, Eunice E. To, Raymond Luong, Felicia Liong, Stella Liong, Osezua Oseghale, Mark A. Miles, Steven Bozinovski, Robert D. Brooks, Ross Vlahos, Stanley Chan, John J. O’Leary, Doug A. Brooks and Stavros Selemidis
Antioxidants 2022, 11(8), 1488; https://doi.org/10.3390/antiox11081488 - 29 Jul 2022
Cited by 13 | Viewed by 2283
Abstract
Macrophages undergo a metabolic switch from oxidative phosphorylation to glycolysis when exposed to gram-negative bacterial lipopolysaccharide (LPS), which modulates antibacterial host defence mechanisms. Here, we show that LPS treatment of macrophages increased the classical oxidative burst response via the NADPH oxidase (NOX) 2 [...] Read more.
Macrophages undergo a metabolic switch from oxidative phosphorylation to glycolysis when exposed to gram-negative bacterial lipopolysaccharide (LPS), which modulates antibacterial host defence mechanisms. Here, we show that LPS treatment of macrophages increased the classical oxidative burst response via the NADPH oxidase (NOX) 2 enzyme, which was blocked by 2-deoxyglucose (2-DG) inhibition of glycolysis. The inhibition of the pentose phosphate pathway with 6-aminonicotinamide (6-AN) also suppressed the LPS-induced increase in NOX2 activity and was associated with a significant reduction in the mRNA expression of NOX2 and its organizer protein p47phox. Notably, the LPS-dependent enhancement in NOX2 oxidase activity was independent of both succinate and mitochondrial reactive oxygen species (ROS) production. LPS also increased type I IFN-β expression, which was suppressed by 2-DG and 6-AN and, therefore, is dependent on glycolysis and the pentose phosphate pathway. The type I IFN-β response to LPS was also inhibited by apocynin pre-treatment, suggesting that NOX2-derived ROS promotes the TLR4-induced response to LPS. Moreover, recombinant IFN-β increased NOX2 oxidase-dependent ROS production, as well as NOX2 and p47phox expression. Our findings identify a previously undescribed molecular mechanism where both glycolysis and the pentose phosphate pathway are required to promote LPS-induced inflammation in macrophages. Full article
(This article belongs to the Special Issue Redox Regulation of the Innate Immunity and Aging)
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