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Biological Role of Oxidative Stress in Inflammatory Diseases

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 36801

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Special Issue Editors

Dr. Sara Franceschelli

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Guest Editor

Department of Medicine and Science of Aging, University “G. D’Annunzio”, 66100 Chieti Pescara, Italy
Interests: nutrition; cellular biology; oxidative stress; cardiovascular disease; endogenous antioxidant enzymes; bioactive vegetable; molecules
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Prof. Dr. Lorenza Speranza

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Guest Editor

Department of Medicine and Science of Aging, University "G. D’Annunzio", 66100 Chieti Pescara, Italy
Interests: oxidative stress; cellular biology; disease; network antioxidant; bioactive vegetable; endogenous antioxidant enzymes; inflammation; nutrition; translation medicine; life sciences
Special Issues, Collections and Topics in MDPI journals

Dr. Chiara D’Angelo

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Assistant Guest Editor

Dept Medical, Oral and Biotechnological Sciences University “G. D’Annunzio” Chieti-Pescara, Italy
Interests: inflammation; gel electrophoresis; agarose gel electrophoresis; neurodegeneration; neurodegenerative diseases

Special Issue Information

Dear Colleagues,

The imbalance between reactive oxidant species and endogenous antioxidant defense mechanisms promotes the development of a condition of oxidative stress, which has considerable biological consequences. Increasing evidence is proving that oxidative stress plays a pivotal role in the development and progression of inflammation, and thus contributes to the pathophysiology of a number of diseases, such as cancer, cardiovascular diseases, diabetes, and neurodegenerative processes.

Oxidant species influence all phases of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals. Their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families leads to activation of signaling pathways promoting the adaptive cellular response to such signals.

While we tend to describe oxidative stress simply as harmful for the human body, it is also true that it is exploited as a therapeutic approach to treat clinical conditions such as cancer, with a certain degree of clinical success.

We can conclude that oxidative stress, although being one of the major injuries to individuals' wellness and health, can also be exploited as a treatment tool.

Therefore, correlations between oxidative stress, inflammation, and disease should be carefully investigated in order to better understand the etiopathogenesis of diseases and to develop ad hoc future treatments.

Prof. Dr. Sara Franceschelli
Prof. Lorenza Speranza
Guest Editors
Dr. Chiara D’Angelo
Assistant Guest Editor

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Published Papers (9 papers)

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Research

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17 pages, 4814 KiB

Open AccessArticle

Dioleoylphosphatidylglycerol Inhibits Heat Shock Protein B4 (HSPB4)-Induced Inflammatory Pathways In Vitro

by Teresa E. Fowler, Vivek Choudhary, Samuel Melnyk, Mishma Farsi, Luke Y. Chang, Nyemkuna Fortingo, Xunsheng Chen, Mitchell A. Watsky and Wendy B. Bollag

Int. J. Mol. Sci. 2023, 24(6), 5839; https://doi.org/10.3390/ijms24065839 - 19 Mar 2023

Cited by 1 | Viewed by 1486

Abstract

Our previous work shows that dioleoylphosphatidylglycerol (DOPG) accelerates corneal epithelial healing in vitro and in vivo by unknown mechanisms. Prior data demonstrate that DOPG inhibits toll-like receptor (TLR) activation and inflammation induced by microbial components (pathogen-associated molecular patterns, PAMPs) and by endogenous molecules upregulated in psoriatic skin, which act as danger-associated molecular patterns (DAMPs) to activate TLRs and promote inflammation. In the injured cornea, sterile inflammation can result from the release of the DAMP molecule, heat shock protein B4 (HSPB4), to contribute to delayed wound healing. Here, we show in vitro that DOPG inhibits TLR2 activation induced in response to HSPB4, as well as DAMPs that are elevated in diabetes, a disease that also slows corneal wound healing. Further, we show that the co-receptor, cluster of differentiation-14 (CD14), is necessary for PAMP/DAMP-induced activation of TLR2, as well as of TLR4. Finally, we simulated the high-glucose environment of diabetes to show that elevated glucose levels enhance TLR4 activation by a DAMP known to be upregulated in diabetes. Together, our results demonstrate the anti-inflammatory actions of DOPG and support further investigation into its development as a possible therapy for corneal injury, especially in diabetic patients at high risk of vision-threatening complications. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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14 pages, 1947 KiB

Open AccessArticle

Microbe-Derived Antioxidants Alleviate Liver and Adipose Tissue Lipid Disorders and Metabolic Inflammation Induced by High Fat Diet in Mice

by Qingying Gao, Zhen Luo, Sheng Ma, Chengbing Yu, Cheng Shen, Weina Xu, Jing Zhang, Hongcai Zhang and Jianxiong Xu

Int. J. Mol. Sci. 2023, 24(4), 3269; https://doi.org/10.3390/ijms24043269 - 07 Feb 2023

Cited by 3 | Viewed by 1880

Abstract

Obesity induces lipodystrophy and metabolic inflammation. Microbe-derived antioxidants (MA) are novel small-molecule nutrients obtained from microbial fermentation, and have anti-oxidation, lipid-lowering and anti-inflammatory effects. Whether MA can regulate obesity-induced lipodystrophy and metabolic inflammation has not yet been investigated. The aim of this study was to investigate the effects of MA on oxidative stress, lipid disorders, and metabolic inflammation in liver and epididymal adipose tissues (EAT) of mice fed with a high-fat diet (HFD). Results showed that MA was able to reverse the HFD-induced increase in body weight, body fat rate and Lee’s index in mice; reduce the fat content in serum, liver and EAT; and regulate the INS, LEP and resistin adipokines as well as free fatty acids to their normal levels. MA also reduced de novo synthesis of fat in the liver and EAT and promoted gene expression for lipolysis, fatty acid transport and β-oxidation. MA decreased TNF-α and MCP1 content in serum, elevated SOD activity in liver and EAT, induced macrophage polarization toward the M2 type, inhibited the NLRP3 pathway, increased gene expression of the anti-inflammatory factors IL-4 and IL-13 and suppressed gene expression of the pro-inflammatory factors IL-6, TNF-α and MCP1, thereby attenuating oxidative stress and inflammation induced by HFD. In conclusion, MA can effectively reduce HFD-induced weight gain and alleviate obesity-induced oxidative stress, lipid disorders and metabolic inflammation in the liver and EAT, indicating that MA shows great promise as a functional food. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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14 pages, 3320 KiB

Open AccessArticle

Metalloendopeptidase ADAM-like Decysin 1 (ADAMDEC1) in Colonic Subepithelial PDGFRα⁺ Cells Is a New Marker for Inflammatory Bowel Disease

by Se Eun Ha, Brian G. Jorgensen, Lai Wei, Byungchang Jin, Min-Seob Kim, Sandra M. Poudrier, Rajan Singh, Allison Bartlett, Hannah Zogg, Sei Kim, Gain Baek, Masaaki Kurahashi, Moon-Young Lee, Yong-Sung Kim, Suck-Chei Choi, Kent C. Sasse, Samuel J. S. Rubin, Andres Gottfried-Blackmore, Laren Becker, Aida Habtezion, Kenton M. Sanders and Seungil Ro Show full author list Hide full author list

Int. J. Mol. Sci. 2022, 23(9), 5007; https://doi.org/10.3390/ijms23095007 - 30 Apr 2022

Cited by 5 | Viewed by 2201

Abstract

Metalloendopeptidase ADAM-Like Decysin 1 (ADAMDEC1) is an anti-inflammatory peptidase that is almost exclusively expressed in the gastrointestinal (GI) tract. We have recently found abundant and selective expression of Adamdec1 in colonic mucosal PDGFRα⁺ cells. However, the cellular origin for this gene expression is controversial as it is also known to be expressed in intestinal macrophages. We found that Adamdec1 mRNAs were selectively expressed in colonic mucosal subepithelial PDGFRα⁺ cells. ADAMDEC1 protein was mainly released from PDGFRα⁺ cells and accumulated in the mucosal layer lamina propria space near the epithelial basement membrane. PDGFRα⁺ cells significantly overexpressed Adamdec1 mRNAs and protein in DSS-induced colitis mice. Adamdec1 was predominantly expressed in CD45⁻ PDGFRα⁺ cells in DSS-induced colitis mice, with only minimal expression in CD45⁺ CD64⁺ macrophages. Additionally, overexpression of both ADAMDEC1 mRNA and protein was consistently observed in PDGFRα⁺ cells, but not in CD64⁺ macrophages found in human colonic mucosal tissue affected by Crohn’s disease. In summary, PDGFRα⁺ cells selectively express ADAMDEC1, which is localized to the colon mucosa layer. ADAMDEC1 expression significantly increases in DSS-induced colitis affected mice and Crohn’s disease affected human tissue, suggesting that this gene can serve as a diagnostic and/or therapeutic target for intestinal inflammation and Crohn’s disease. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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12 pages, 4650 KiB

Open AccessArticle

Oxidative Stress and Inflammatory Biomarkers for the Prediction of Severity and ICU Admission in Unselected Patients Hospitalized with COVID-19

by Morgane Ducastel, Camille Chenevier-Gobeaux, Yassine Ballaa, Jean-François Meritet, Michel Brack, Nicolas Chapuis, Frédéric Pene, Nicolas Carlier, Tali-Anne Szwebel, Nicolas Roche, Benjamin Terrier and Didier Borderie

Int. J. Mol. Sci. 2021, 22(14), 7462; https://doi.org/10.3390/ijms22147462 - 12 Jul 2021

Cited by 37 | Viewed by 2667

Abstract

Objective: We aimed to investigate the prognostic performances of oxidative stress (OS), inflammatory and cell activation biomarkers measured at admission in COVID-19 patients. Design: retrospective monocentric study. Setting: patients with suspected SARS-CoV-2 infection (COVID-19) admitted to the hospital. Patients: One hundred and sixty documented and unselected COVID-19-patients. Disease severity (from mild to critical) was scored according to NIH’s classification. Interventions: none. Measurements and main results: We measured OS biomarkers (thiol, advanced oxidation protein products (AOPP), ischemia-modified albumin (IMA)), inflammation biomarkers (interleukin-6 (IL-6), presepsin) and cellular activation biomarkers (calprotectin) in plasma at admission. Thiol concentrations decreased while IMA, IL-6, calprotectin and PSEP increased with disease severity in COVID-19 patients and were associated with increased O₂ needs and ICU admission. The best area under the receiver-operating-characteristics curve (AUC) for the prediction of ICU admission was for thiol (AUC = 0.762). A thiol concentration <154 µmol/L was predictive for ICU admission (79.7% sensitivity, 64.6% specificity, 58.8% positive predictive value, 78.9% negative predictive value). In a stepwise logistic regression, we found that being overweight, having dyspnoea, and thiol and IL-6 plasmatic concentrations were independently associated with ICU admission. In contrast, calprotectin was the best biomarker to predict mortality (AUC = 0.792), with an optimal threshold at 24.1 mg/L (94.1% sensitivity, 64.9% specificity, 97.1% positive predictive value and 98.9% negative predictive value), and survival curves indicated that high IL-6 and calprotectin concentrations were associated with a significantly increased risk of mortality. Conclusions: Thiol measurement at admission is a promising tool to predict ICU admission in COVID-19-patients, whereas IL-6 and calprotectin measurements effectively predict mortality. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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Review

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22 pages, 2931 KiB

Open AccessReview

An Overview of Oxidative Stress, Neuroinflammation, and Neurodegenerative Diseases

by Daniel Mihai Teleanu, Adelina-Gabriela Niculescu, Iulia Ioana Lungu, Crina Ioana Radu, Oana Vladâcenco, Eugenia Roza, Bogdan Costăchescu, Alexandru Mihai Grumezescu and Raluca Ioana Teleanu

Int. J. Mol. Sci. 2022, 23(11), 5938; https://doi.org/10.3390/ijms23115938 - 25 May 2022

Cited by 182 | Viewed by 9048

Abstract

Oxidative stress has been linked with a variety of diseases, being involved in the debut and/or progress of several neurodegenerative disorders. This review intends to summarize some of the findings that correlate the overproduction of reactive oxygen species with the pathophysiology of Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Oxidative stress was also noted to modify the inflammatory response. Even though oxidative stress and neuroinflammation are two totally different pathological events, they are linked and affect one another. Nonetheless, there are still several mechanisms that need to be understood regarding the onset and the progress of neurodegenerative diseases in order to develop efficient therapies. As antioxidants are a means to alter oxidative stress and slow down the symptoms of these neurodegenerative diseases, the most common antioxidants, enzymatic as well as non-enzymatic, have been mentioned in this paper as therapeutic options for the discussed disorders. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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17 pages, 620 KiB

Open AccessReview

The Role of Oxidative Stress in Sarcoidosis

by Sara Solveig Fois, Sara Canu and Alessandro Giuseppe Fois

Int. J. Mol. Sci. 2021, 22(21), 11712; https://doi.org/10.3390/ijms222111712 - 28 Oct 2021

Cited by 4 | Viewed by 2443

Abstract

Sarcoidosis is a rare, systemic inflammatory disease whose diagnosis and management can pose a challenge for clinicians and specialists. Scientific knowledge on the molecular pathways that drive its development is still lacking, with no standardized therapies available and insufficient strategies to predict patient outcome. In recent years, oxidative stress has been highlighted as an important factor in the pathogenesis of sarcoidosis, involving several enzymes and molecules in the mechanism of the disease. This review presents current data on the role of oxidative stress in sarcoidosis and its interaction with inflammation, as well as the application of antioxidative therapy in the disease. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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20 pages, 13058 KiB

Open AccessReview

Roles of PRR-Mediated Signaling Pathways in the Regulation of Oxidative Stress and Inflammatory Diseases

by Pengwei Li and Mingxian Chang

Int. J. Mol. Sci. 2021, 22(14), 7688; https://doi.org/10.3390/ijms22147688 - 19 Jul 2021

Cited by 48 | Viewed by 6017

Abstract

Oxidative stress is a major contributor to the pathogenesis of various inflammatory diseases. Accumulating evidence has shown that oxidative stress is characterized by the overproduction of reactive oxygen species (ROS). Previous reviews have highlighted inflammatory signaling pathways, biomarkers, molecular targets, and pathogenetic functions mediated by oxidative stress in various diseases. The inflammatory signaling cascades are initiated through the recognition of host cell-derived damage associated molecular patterns (DAMPs) and microorganism-derived pathogen associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs). In this review, the effects of PRRs from the Toll-like (TLRs), the retinoic acid-induced gene I (RIG-I)-like receptors (RLRs) and the NOD-like (NLRs) families, and the activation of these signaling pathways in regulating the production of ROS and/or oxidative stress are summarized. Furthermore, important directions for future studies, especially for pathogen-induced signaling pathways through oxidative stress are also reviewed. The present review will highlight potential therapeutic strategies relevant to inflammatory diseases based on the correlations between ROS regulation and PRRs-mediated signaling pathways. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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12 pages, 701 KiB

Open AccessReview

Molecular Hydrogen as a Novel Protective Agent against Pre-Symptomatic Diseases

by Haru Yamamoto, Yusuke Ichikawa, Shin-ichi Hirano, Bunpei Sato, Yoshiyasu Takefuji and Fumitake Satoh

Int. J. Mol. Sci. 2021, 22(13), 7211; https://doi.org/10.3390/ijms22137211 - 05 Jul 2021

Cited by 7 | Viewed by 4956

Abstract

Mibyou, or pre-symptomatic diseases, refers to state of health in which a disease is slowly developing within the body yet the symptoms are not apparent. Common examples of mibyou in modern medicine include inflammatory diseases that are caused by chronic inflammation. It is known that chronic inflammation is triggered by the uncontrolled release of proinflammatory cytokines by neutrophils and macrophages in the innate immune system. In a recent study, it was shown that molecular hydrogen (H₂) has the ability to treat chronic inflammation by eliminating hydroxyl radicals (·OH), a mitochondrial reactive oxygen species (ROS). In doing so, H₂ suppresses oxidative stress, which is implicated in several mechanisms at the root of chronic inflammation, including the activation of NLRP3 inflammasomes. This review explains these mechanisms by which H₂ can suppress chronic inflammation and studies its applications as a protective agent against different inflammatory diseases in their pre-symptomatic state. While mibyou cannot be detected nor treated by modern medicine, H₂ is able to suppress the pathogenesis of pre-symptomatic diseases, and thus exhibits prospects as a novel protective agent. Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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12 pages, 789 KiB

Open AccessReview

Potential Therapeutic Applications of Hydrogen in Chronic Inflammatory Diseases: Possible Inhibiting Role on Mitochondrial Stress

by Shin-ichi Hirano, Yusuke Ichikawa, Bunpei Sato, Haru Yamamoto, Yoshiyasu Takefuji and Fumitake Satoh

Int. J. Mol. Sci. 2021, 22(5), 2549; https://doi.org/10.3390/ijms22052549 - 04 Mar 2021

Cited by 22 | Viewed by 4708

Abstract

Mitochondria are the largest source of reactive oxygen species (ROS) and are intracellular organelles that produce large amounts of the most potent hydroxyl radical (·OH). Molecular hydrogen (H₂) can selectively eliminate ·OH generated inside of the mitochondria. Inflammation is induced by the release of proinflammatory cytokines produced by macrophages and neutrophils. However, an uncontrolled or exaggerated response often occurs, resulting in severe inflammation that can lead to acute or chronic inflammatory diseases. Recent studies have reported that ROS activate NLRP3 inflammasomes, and that this stimulation triggers the production of proinflammatory cytokines. It has been shown in literature that H₂ can be based on the mechanisms that inhibit mitochondrial ROS. However, the ability for H₂ to inhibit NLRP3 inflammasome activation via mitochondrial oxidation is poorly understood. In this review, we hypothesize a possible mechanism by which H₂ inhibits mitochondrial oxidation. Medical applications of H₂ may solve the problem of many chronic inflammation-based diseases, including coronavirus disease 2019 (COVID-19). Full article

(This article belongs to the Special Issue Biological Role of Oxidative Stress in Inflammatory Diseases)

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