Special Issue "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 2527

Special Issue 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

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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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Research

Article
Peroxiredoxins Play an Important Role in the Regulation of Immunity and Aging in Drosophila
Antioxidants 2023, 12(8), 1616; https://doi.org/10.3390/antiox12081616 - 15 Aug 2023
Viewed by 435
Abstract
Aberrant immune responses and chronic inflammation can impose significant health risks and promote premature aging. Pro-inflammatory responses are largely mediated via reactive oxygen species (ROS) and reduction–oxidation reactions. A pivotal role in maintaining cellular redox homeostasis and the proper control of redox-sensitive signaling [...] Read more.
Aberrant immune responses and chronic inflammation can impose significant health risks and promote premature aging. Pro-inflammatory responses are largely mediated via reactive oxygen species (ROS) and reduction–oxidation reactions. A pivotal role in maintaining cellular redox homeostasis and the proper control of redox-sensitive signaling belongs to a family of antioxidant and redox-regulating thiol-related peroxidases designated as peroxiredoxins (Prx). Our recent studies in Drosophila have shown that Prxs play a critical role in aging and immunity. We identified two important ‘hubs’, the endoplasmic reticulum (ER) and mitochondria, where extracellular and intracellular stress signals are transformed into pro-inflammatory responses that are modulated by the activity of the Prxs residing in these cellular organelles. Here, we found that mitochondrial Prx activity in the intestinal epithelium is required to prevent the development of intestinal barrier dysfunction, which can drive systemic inflammation and premature aging. Using a redox-negative mutant, we demonstrated that Prx acts in a redox-dependent manner in regulating the age-related immune response. The hyperactive immune response observed in flies under-expressing mitochondrial Prxs is due to a response to abiotic signals but not to changes in the bacterial content. This hyperactive response, but not reduced lifespan phenotype, can be rescued by the ER-localized Prx. Full article
(This article belongs to the Special Issue Redox Regulation of the Innate Immunity and Aging)
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Article
Glycolysis and the Pentose Phosphate Pathway Promote LPS-Induced NOX2 Oxidase- and IFN-β-Dependent Inflammation in Macrophages
Antioxidants 2022, 11(8), 1488; https://doi.org/10.3390/antiox11081488 - 29 Jul 2022
Cited by 6 | Viewed by 1624
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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