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Antioxidants
Special Issues
Oxidative Stress in Rheumatic Diseases
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Oxidative Stress in Rheumatic Diseases

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 (15 July 2023) | Viewed by 7419

Special Issue Editors

Dr. Bruna Miglioranza Scavuzzi

E-Mail Website
Guest Editor
Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA
Interests: oxidative stress; antioxidants; inflammation; autoimmune disorders; mitochondria
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Joseph Holoshitz

E-Mail Website
Guest Editor
Division of Rheumatology, University of Michigan School of Medicine, Ann Arbor, MI 48109-5680, USA
Interests: clinical and experimental autoimmunity; immunogenetics; mechanisms of major histocompatibility complex-associated diseases; oxidative stress and its role in autoimmune conditions; signaling pathway aberrations in rheumatoid arthritis and lupus; immune regulation; clinical and translational research in rheumatoid arthritis and lupus; osteoimmunology; new therapeutic strategies for bone disease and arthritis

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) are constitutive products of cellular metabolism which are required for signaling pathways that regulate physiological cell function. However, when imbalance between ROS production and their elimination occurs, they may accumulate and become pathogenic, causing oxidative stress, which plays an important role in several inflammatory and autoimmune diseases. Recent advances in our understanding of the pathological action of ROS, as well as promising findings involving prevention or treatment of rheumatic diseases with antioxidant therapies, have highlighted the potential of redox homeostasis for the maintenance of physiological functions and the prevention of redox-dependent pathologies.

In the second volume of this Special Issue, we plan to focus on updated research findings concerning the role of oxidative stress in systemic lupus erythematosus, rheumatoid arthritis, and other rheumatic diseases. In vitro studies investigating molecular mechanisms, in vivo studies involving oxidative stress biomarkers, as well as the effect of the therapeutic effects of antioxidants will be considered for this issue. Both original and review articles are welcome.

Dr. Bruna Miglioranza Scavuzzi
Prof. Dr. Joseph Holoshitz
Guest Editors

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.

Published Papers (4 papers)

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Research

12 pages, 4148 KiB  
Article
Biomarkers of Oxidative Stress in Systemic Lupus Erythematosus Patients with Active Nephritis
by Lu Liu, Karina de Leeuw, Suzanne Arends, Berber Doornbos-van der Meer, Marian L. C. Bulthuis, Harry van Goor and Johanna Westra
Antioxidants 2023, 12(8), 1627; https://doi.org/10.3390/antiox12081627 - 17 Aug 2023
Cited by 2 | Viewed by 1053
Abstract
Oxidative stress plays an important role in systemic lupus erythematosus (SLE) and especially in lupus nephritis (LN). The aim of this study was to compare redox-related biomarkers between patients with active LN, quiescent SLE (Q-SLE) and healthy controls (HC) and to explore their [...] Read more.
Oxidative stress plays an important role in systemic lupus erythematosus (SLE) and especially in lupus nephritis (LN). The aim of this study was to compare redox-related biomarkers between patients with active LN, quiescent SLE (Q-SLE) and healthy controls (HC) and to explore their association with clinical characteristics such as disease activity in patients. We investigated levels of plasma free thiols (R-SH, sulfhydryl groups), levels of soluble receptor for advanced glycation end products (sRAGE) and levels of malondialdehyde (MDA) in SLE patients with active LN (n = 23), patients with quiescent SLE (n = 47) and HC (n = 23). Data of LN patients who previously participated in Dutch lupus nephritis studies and longitudinal samples up to 36 months were analyzed. Thiol levels were lower in active LN at baseline and Q-SLE patients compared to HC. In generalized estimating equation (GEE) modelling, free thiol levels were negatively correlated with the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) over time (p < 0.001). sRAGE and MDA were positively correlated with the SLEDAI over time (p = 0.035 and p = 0.016, respectively). These results indicate that oxidative stress levels in LN patients are increased compared to HC and associated with SLE disease activity. Therefore, interventional therapy to restore redox homeostasis may be useful as an adjunctive therapy in the treatment of oxidative damage in SLE. Full article
(This article belongs to the Special Issue Oxidative Stress in Rheumatic Diseases)
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15 pages, 6522 KiB  
Article
Human NCF190H Variant Promotes IL-23/IL-17—Dependent Mannan-Induced Psoriasis and Psoriatic Arthritis
by Yanpeng Li, Zhilei Li, Kutty Selva Nandakumar and Rikard Holmdahl
Antioxidants 2023, 12(7), 1348; https://doi.org/10.3390/antiox12071348 - 27 Jun 2023
Cited by 3 | Viewed by 1691
Abstract
Recently, a major single nucleotide variant on the NCF1 gene, leading to an amino acid replacement from arginine to histidine at position 90 (NCF1R90H), associated with low production of reactive oxygen species (ROS), was found to be causative for several autoimmune [...] Read more.
Recently, a major single nucleotide variant on the NCF1 gene, leading to an amino acid replacement from arginine to histidine at position 90 (NCF1R90H), associated with low production of reactive oxygen species (ROS), was found to be causative for several autoimmune diseases. Psoriasis in the skin (PsO) and psoriatic arthritis (PsA) were induced with mannan by intraperitoneal injection or epicutaneous application, evaluated by visual and histology scoring. Immunostaining was used to identify macrophages, NCF1, and keratinocytes. The population of immune cells was quantified by flow cytometry, gene expression was analyzed by RT-qPCR, and the JAK/STAT signaling pathway was investigated by immunohistochemical staining and western blot. We found that the low ROS responder NCF190H variant promotes PsO and PsA (the MIP model). The NCF190H-expressing mice had hyperactivated macrophages, expanded keratinocytes, and dramatically increased numbers of γδT17 cells with upregulated IL-17A, IL-23, and TNF-α. In addition, the JAK1/STAT3 signaling pathway was also upregulated in cells in the psoriatic skin tissues of Ncf190H mice. To summarize, a defined SNP (NCF1-339, also named NCF190H) was found to activate the IL-23/IL-17 axis and JAK-STAT signaling pathways, leading to hyperactivation of macrophages and keratinocytes and causing mouse psoriasis and psoriatic arthritis. Full article
(This article belongs to the Special Issue Oxidative Stress in Rheumatic Diseases)
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21 pages, 3655 KiB  
Article
IL-21, Inflammatory Cytokines and Hyperpolarized CD8+ T Cells Are Central Players in Lupus Immune Pathology
by Soumya Sengupta, Gargee Bhattacharya, Subhasmita Mohanty, Shubham K. Shaw, Gajendra M. Jogdand, Rohila Jha, Prakash K. Barik, Jyoti R. Parida and Satish Devadas
Antioxidants 2023, 12(1), 181; https://doi.org/10.3390/antiox12010181 - 12 Jan 2023
Cited by 2 | Viewed by 2244
Abstract
Systemic lupus erythematous (SLE) is a chronic autoimmune disorder, broadly characterized by systemic inflammation along with heterogeneous clinical manifestations, severe morbidity, moribund organ failure and eventual mortality. In our study, SLE patients displayed a higher percentage of activated, inflamed and hyper-polarized CD8+ [...] Read more.
Systemic lupus erythematous (SLE) is a chronic autoimmune disorder, broadly characterized by systemic inflammation along with heterogeneous clinical manifestations, severe morbidity, moribund organ failure and eventual mortality. In our study, SLE patients displayed a higher percentage of activated, inflamed and hyper-polarized CD8+ T cells, dysregulated CD8+ T cell differentiation, significantly elevated serum inflammatory cytokines and higher accumulation of cellular ROS when compared to healthy controls. Importantly, these hyper-inflammatory/hyper-polarized CD8+ T cells responded better to an antioxidant than to an oxidant. Terminally differentiated Tc1 cells also showed plasticity upon oxidant/antioxidant treatment, but that was in contrast to the SLE CD8+ T cell response. Our studies suggest that the differential phenotype and redox response of SLE CD8+ T cells and Tc1 cells could be attributed to their cytokine environs during their respective differentiation and eventual activation environs. The polarization of Tc1 cells with IL-21 drove hyper-cytotoxicity without hyper-polarisation suggesting that the SLE inflammatory cytokine environment could drive the extreme aberrancy in SLE CD8+ T cells. Full article
(This article belongs to the Special Issue Oxidative Stress in Rheumatic Diseases)
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17 pages, 2590 KiB  
Article
NRF2/Itaconate Axis Regulates Metabolism and Inflammatory Properties of T Cells in Children with JIA
by Anandhi Rajendiran, Sudheendra Hebbar Subramanyam, Patricia Klemm, Vera Jankowski, Jorg van Loosdregt, Bas Vastert, Kristina Vollbach, Norbert Wagner, Klaus Tenbrock and Kim Ohl
Antioxidants 2022, 11(12), 2426; https://doi.org/10.3390/antiox11122426 - 08 Dec 2022
Cited by 3 | Viewed by 1844
Abstract
Background: CD4+ T cells critically contribute to the initiation and perturbation of inflammation. When CD4+ T cells enter inflamed tissues, they adapt to hypoxia and oxidative stress conditions, and to a reduction in nutrients. We aimed to investigate how this distinct environment regulates [...] Read more.
Background: CD4+ T cells critically contribute to the initiation and perturbation of inflammation. When CD4+ T cells enter inflamed tissues, they adapt to hypoxia and oxidative stress conditions, and to a reduction in nutrients. We aimed to investigate how this distinct environment regulates T cell responses within the inflamed joints of patients with childhood rheumatism (JIA) by analyzing the behavior of NRF2—the key regulator of the anti-oxidative stress response—and its signaling pathways. Methods: Flow cytometry and quantitative RT-PCR were used to perform metabolic profiling of T cells and to measure the production of inflammatory cytokines. Loss of function analyses were carried out by means of siRNA transfection experiments. NRF2 activation was induced by treatment with 4-octyl-Itaconate (4-OI). Results: Flow cytometry analyses revealed a high metabolic status in CD4+ T cells taken from synovial fluid (SF) with greater mitochondrial mass, and increased glucose and fatty acid uptake. This resulted in a heightened oxidative status of SF CD4+ T cells. Despite raised ROS levels, expression of NRF2 and its target gene NQO1 were lower in CD4+ T cells from SF than in those from blood. Indeed, NRF2 activation of CD4+ T cells downregulated oxidative stress markers, altered the metabolic phenotype and reduced secretion of IFN-γ. Conclusion: NRF2 could be a potential regulator in CD4+ T cells during chronic inflammation and could instigate a drift toward disease progression or regression, depending on the inflammatory environment. Full article
(This article belongs to the Special Issue Oxidative Stress in Rheumatic Diseases)
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