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Antioxidants
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Oxidative Stress in Respiratory Diseases
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Oxidative Stress in Respiratory 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 September 2024) | Viewed by 20625

Special Issue Editors

Dr. Sabina Galiniak

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Guest Editor
Institute of Medical Sciences, Rzeszów University, Rzeszów, Poland
Interests: biomarkers; inflammation; oxidative stress; molecular biology
Special Issues, Collections and Topics in MDPI journals
Prof. Marta Rachel

E-Mail Website
Guest Editor
1. Institute of Medical Sciences, Medical College, Rzeszow University, Warzywna 1a, 35-310 Rzeszow, Poland
2. State Hospital 2 in Rzeszów, Lwowska 60, 35-301 Rzeszów, Poland
Interests: allergic rhinitis; allergy; asthma in children and adolescents; cystic fibrosis; immunotherapy of insect venoms; nitric oxide
Prof. Dr. Stephen M. Black

E-Mail Website
Guest Editor
Department of Cellular Biology & Pharmacology, Florida International University, Miami, FL, USA
Interests: lung diseases; respiratory physiology; pulmonary hypertension; lung vascular pathobiology; reactive Oxygen Species (ROS); nitric oxide; Nitric Oxide Synthase (eNOS); NO signaling; endothelial dysfunction

Special Issue Information

Dear Colleagues,

Oxidative stress is defined as an imbalance between the increased production of reactive oxygen species (ROS) and reduced or defective antioxidant mechanisms. Oxidative stress plays a significant role in the development and maintenance of the inflammatory process that occurs in the course of respiratory diseases such as cystic fibrosis, allergic rhinitis, asthma, and chronic obstructive pulmonary disease. Moreover, oxidative stress leads to direct tissue damage as well as worsening of lung function, bronchial wall edema, constriction of the bronchioles and smaller airways, and excessive mucus secretion.

In this Special Issue, we invite you to submit original research papers, review articles, and clinical trial results related to any aspect of the assessment and role of oxidative and nitrosative stress in the pathogenesis of respiratory diseases and antioxidant therapeutic approaches.

We look forward to your contribution.

Dr. Sabina Galiniak
Dr. Marta Rachel
Prof. Dr. Stephen Black
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.

Keywords

  • oxidative stress
  • asthma
  • cystic fibrosis
  • chronic obstructive pulmonary disease

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Published Papers (7 papers)

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Research

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13 pages, 3974 KiB  
Article
Armillaria mellea Mycelia Alleviate PM2.5-Induced Pulmonary Inflammation in Murine Models
by Yi-Ping Huang, Yu-Tsen Huang, Hui-Yu Wu, Li-Fang Chou, You-Shan Tsai, Yih-Min Jiang, Wan-Ping Chen, Ting-Wei Lin, Chin-Chu Chen and Chih-Ho Lai
Antioxidants 2024, 13(11), 1381; https://doi.org/10.3390/antiox13111381 - 12 Nov 2024
Viewed by 402
Abstract
Particulate matter (PM) with an aerodynamic diameter of ≤2.5 μm (PM2.5) significantly contributes to various disease-related respiratory inflammations. Armillaria mellea, recognized for its medicinal properties, could alleviate these respiratory ailments. However, its efficacy against PM2.5-induced inflammation remains elusive. In this study, we [...] Read more.
Particulate matter (PM) with an aerodynamic diameter of ≤2.5 μm (PM2.5) significantly contributes to various disease-related respiratory inflammations. Armillaria mellea, recognized for its medicinal properties, could alleviate these respiratory ailments. However, its efficacy against PM2.5-induced inflammation remains elusive. In this study, we investigated whether A. mellea mycelia could mitigate PM2.5-induced respiratory inflammation and assessed the underlying mechanisms. Our results showed that A. mellea mycelia significantly reduced PM2.5-induced nitric oxide (NO) production and nuclear factor (NF)-κB activation in macrophages. Furthermore, A. mellea mycelia suppressed the expression of inflammatory mediators, indicating their potent antioxidant and anti-inflammatory properties. In murine models, A. mellea mycelia mitigated PM2.5-induced lung inflammation and cytokine secretion, restoring lung inflammatory status. Our results highlight the potential of A. mellea mycelia to treat PM2.5-induced respiratory inflammation. The antioxidant and anti-inflammatory effects of A. mellea mycelia demonstrated in vitro and in vivo hold promising potential for developing respiratory health improvement interventions upon PM2.5 exposure. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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13 pages, 17976 KiB  
Article
Nrf2 Deficiency Accelerates IL-17-Dependent Neutrophilic Airway Inflammation in Asthmatic Mice
by Kenya Kuramoto, Yuko Morishima, Kazufumi Yoshida, Satoshi Ano, Kai Kawashima, Yuki Yabuuchi, Chio Sakai, Sosuke Matsumura, Kengo Nishino, Kai Yazaki, Masashi Matsuyama, Takumi Kiwamoto, Yukio Ishii and Nobuyuki Hizawa
Antioxidants 2024, 13(7), 818; https://doi.org/10.3390/antiox13070818 - 8 Jul 2024
Cited by 1 | Viewed by 968
Abstract
Asthma is a heterogeneous disease that can be broadly classified into type 2, which is primarily steroid-sensitive and eosinophilic, and non-type 2, which is primarily steroid-resistant and neutrophilic. While the mechanisms leading to the development of molecular-targeted therapies for type 2 asthma are [...] Read more.
Asthma is a heterogeneous disease that can be broadly classified into type 2, which is primarily steroid-sensitive and eosinophilic, and non-type 2, which is primarily steroid-resistant and neutrophilic. While the mechanisms leading to the development of molecular-targeted therapies for type 2 asthma are being elucidated, much remains to be learned about non-type 2 asthma. To investigate the role of oxidative stress in refractory allergic airway inflammation, we compared asthma models generated by immunizing wild-type and nuclear factor erythroid-2-related factor 2 (Nrf2)-deficient mice with the house dust mite antigen. Both asthma models had similar levels of airway inflammation and hyperresponsiveness, but the Nrf2-deficient mice had increased oxidative stress and exacerbated neutrophilic airway inflammation compared with the wild-type mice. Type 2 cytokines and the expression of GATA3, a transcription factor that is important for Th2 cell differentiation, had decreased in Nrf2-deficient mice compared with the wild-type mice, whereas helper T (Th) 17 cytokines and the expression of RORγt, which is important for Th17 cell differentiation, had increased. Furthermore, the neutrophilic airway inflammation caused by Nrf2 deficiency was ameliorated by interleukin (IL)-17 neutralization. We have concluded that the disruption of the Nrf2-mediated antioxidant defense system contributed to the induction of Th17 differentiation and exacerbated allergic neutrophilic airway inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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11 pages, 1090 KiB  
Communication
Ischemia-Modified Albumin (IMA) Is Associated with Poor Survival in Patients with Newly Diagnosed Idiopathic Pulmonary Fibrosis (IPF): A Pilot Study
by Angelo Zinellu, Stefano Zoroddu, Simona Fois, Sabrina Mellino, Chiara Scala, Erika Virdis, Elisabetta Zinellu, Salvatore Sotgia, Panagiotis Paliogiannis, Arduino A. Mangoni, Ciriaco Carru, Pietro Pirina and Alessandro G. Fois
Antioxidants 2024, 13(3), 278; https://doi.org/10.3390/antiox13030278 - 25 Feb 2024
Cited by 1 | Viewed by 1218
Abstract
There are increasing efforts to better predict adverse outcomes for idiopathic pulmonary fibrosis (IPF). Our aim was to assess the prognostic potential of ischemia-modified albumin (IMA), an established circulating marker of ischemia and, more recently, oxidative stress, in a cohort of 56 IPF [...] Read more.
There are increasing efforts to better predict adverse outcomes for idiopathic pulmonary fibrosis (IPF). Our aim was to assess the prognostic potential of ischemia-modified albumin (IMA), an established circulating marker of ischemia and, more recently, oxidative stress, in a cohort of 56 IPF patients recruited between 2015 and 2023 at the University of Sassari, Italy. Demographic and functional parameters and serum IMA concentrations were measured at baseline. Non-survivors had significantly higher IMA concentrations vs. survivors (508 ± 64 vs. 474 ± 42 mABSU, respectively; p = 0.035). The Kaplan–Meier analysis showed a significant association between higher IMA values and poor survival (HR: 3.32, 95% CI from 1.06 to 10.4, p = 0.039). In the Cox regression analysis, this association remained significant after adjusting for the force expiratory volume at 1 s, the total lung capacity, lymphocyte count, and pharmacological treatment (HR: 1.0154, 95% CI from 1.0035 to 1.0275, p = 0.01). IMA, an oxidative stress biomarker measurable using relatively simple and available methods, is independently associated with mortality in IPF. Therefore, its determination may enhance risk stratification and treatment decisions. Prospective studies involving larger cohorts are needed to confirm this association and to endorse the use of IMA in routine practice. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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19 pages, 9245 KiB  
Article
Itaconate Suppresses the Activation of Mitochondrial NLRP3 Inflammasome and Oxidative Stress in Allergic Airway Inflammation
by Qiu-Meng Xie, Ning Chen, Si-Ming Song, Cui-Cui Zhao, Ya Ruan, Jia-Feng Sha, Qian Liu, Xu-Qin Jiang, Guang-He Fei and Hui-Mei Wu
Antioxidants 2023, 12(2), 489; https://doi.org/10.3390/antiox12020489 - 15 Feb 2023
Cited by 5 | Viewed by 2907
Abstract
Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects [...] Read more.
Itaconate has emerged as a novel anti-inflammatory and antioxidative endogenous metabolite, yet its role in allergic airway inflammation (AAI) and the underlying mechanism remains elusive. Here, the itaconate level in the lung was assessed by High Performance Liquid Chromatography (HPLC), and the effects of the Irg1/itaconate pathway on AAI and alveolar macrophage (AM) immune responses were evaluated using an ovalbumin (OVA)-induced AAI model established by wild type (WT) and Irg1−/− mice, while the mechanism of this process was investigated by metabolomics analysis, mitochondrial/cytosolic protein fractionation and transmission electron microscopy in the lung tissues. The results demonstrated that the Irg1 mRNA/protein expression and itaconate production in the lung were significantly induced by OVA. Itaconate ameliorated while Irg1 deficiency augmented AAI, and this may be attributed to the fact that itaconate suppressed mitochondrial events such as NLRP3 inflammasome activation, oxidative stress and metabolic dysfunction. Furthermore, we identified that the Irg1/itaconate pathway impacted the NLRP3 inflammasome activation and oxidative stress in AMs. Collectively, our findings provide evidence for the first time, supporting the conclusion that in the allergic lung, the itaconate level is markedly increased, which directly regulates AMs’ immune responses. We therefore propose that the Irg1/itaconate pathway in AMs is a potential anti-inflammatory and anti-oxidative therapeutic target for AAI. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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12 pages, 2218 KiB  
Article
Elevated Nitrite/Nitrate Ratio as a Potential Biomarker for the Differential Diagnosis of Pleural Effusions
by Mu-Rong Chao, Yuan-Jhe Chang, Ying-Ming Shih, Jian-Lian Chen, Cheng-Chieh Yen and Chiung-Wen Hu
Antioxidants 2022, 11(7), 1327; https://doi.org/10.3390/antiox11071327 - 6 Jul 2022
Viewed by 2221
Abstract
Pleural effusions (PEs) are common in clinical practice and can be due to many different underlying diseases such as cancer, congestive heart failure, or pneumonia. An accurate differential diagnostic categorization is essential, as the treatment and prognosis of PEs largely depend on its [...] Read more.
Pleural effusions (PEs) are common in clinical practice and can be due to many different underlying diseases such as cancer, congestive heart failure, or pneumonia. An accurate differential diagnostic categorization is essential, as the treatment and prognosis of PEs largely depend on its cause. In this study, we tested the hypothesis that nitrite and nitrate concentrations in PEs are associated with the inflammation and infection conditions. We therefore measured the nitrite and nitrate levels in 143 PE samples using a sensitive liquid chromatography-tandem mass spectrometry method and investigated their diagnostic potential in differentiating PEs. The results showed that nitrite concentrations and nitrite/nitrate ratios were higher in exudates than in transudates (NO2−: 2.12 vs. 1.49 μM; NO2−/NO3−: 23.3 vs. 14.0). Both the nitrite concentrations and the nitrite/nitrate ratios were positively correlated with the three Light’s criteria. Moreover, the receiver operating characteristic curve analysis revealed that the nitrite/nitrate ratio with an area under the curve of 0.71 could be a potential diagnostic biomarker in separating infectious PEs (IPEs) from other types of PEs. Taken together, the nitrite/nitrate ratio not only reflected the statuses of inflammation, but also the nitrate reduction by pathogenic bacteria infection in the pleural cavity. The nitrite/nitrate ratio could be a better biomarker in the differential diagnosis of PEs than the nitrite concentration alone. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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16 pages, 1266 KiB  
Article
Links between Disease Severity, Bacterial Infections and Oxidative Stress in Cystic Fibrosis
by Sabina Galiniak, Mateusz Mołoń and Marta Rachel
Antioxidants 2022, 11(5), 887; https://doi.org/10.3390/antiox11050887 - 29 Apr 2022
Cited by 13 | Viewed by 2615
Abstract
Cystic fibrosis (CF) is one of the most common, yet fatal genetic diseases in Caucasians. The presence of a defective CF transmembrane conductance regulator and the massive neutrophils influx into the airways contribute to an imbalance in epithelial cell processes and extracellular fluids [...] Read more.
Cystic fibrosis (CF) is one of the most common, yet fatal genetic diseases in Caucasians. The presence of a defective CF transmembrane conductance regulator and the massive neutrophils influx into the airways contribute to an imbalance in epithelial cell processes and extracellular fluids and lead to excessive production of reactive oxygen species and intensification of oxidative stress. The study included 16 controls and 42 participants with CF aged 10 to 38. The products of protein oxidation, total antioxidant capacity (TAC) and markers of lipid peroxidation were estimated in the serum of the subjects. Furthermore, we compared the level of oxidative stress in patients with CF according to the severity of disease and type of bacterial infection. Thiol groups and serum TAC decreased significantly in patients with CF (p < 0.05). Elevated levels of 3-nitrotyrosine, malondialdehyde and 8-isoprostane were observed in CF subjects (p < 0.05). Furthermore, as the severity of the disease increased, there was a decrease in the thiol groups and TAC levels, as well as an increase in the concentration of 3-nitrotyrosine and 8-isoprostane. CF participants infected with Pseudomonas aeruginosa had elevated 3-nitrotyrosine concentration levels (p < 0.05), while those infected with Staphylococcus aureus noted a decrease in thiol groups (p < 0.05). Elevated levels of oxidative stress markers were found in the serum of CF patients. Furthermore, oxidative stress progressively increased over the years and along with the severity of the disease. The presence of bacterial infection with P. aeruginosa or S. aureus had a slight effect on oxidative stress, while co-infection by two species did not affect the level of oxidative stress. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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Review

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28 pages, 8119 KiB  
Review
The Impact of Tobacco Cigarettes, Vaping Products and Tobacco Heating Products on Oxidative Stress
by Rosalia Emma, Massimo Caruso, Davide Campagna, Roberta Pulvirenti and Giovanni Li Volti
Antioxidants 2022, 11(9), 1829; https://doi.org/10.3390/antiox11091829 - 16 Sep 2022
Cited by 20 | Viewed by 8301
Abstract
Cells constantly produce oxidizing species because of their metabolic activity, which is counteracted by the continuous production of antioxidant species to maintain the homeostasis of the redox balance. A deviation from the metabolic steady state leads to a condition of oxidative stress. The [...] Read more.
Cells constantly produce oxidizing species because of their metabolic activity, which is counteracted by the continuous production of antioxidant species to maintain the homeostasis of the redox balance. A deviation from the metabolic steady state leads to a condition of oxidative stress. The source of oxidative species can be endogenous or exogenous. A major exogenous source of these species is tobacco smoking. Oxidative damage can be induced in cells by chemical species contained in smoke through the generation of pro-inflammatory compounds and the modulation of intracellular pro-inflammatory pathways, resulting in a pathological condition. Cessation of smoking reduces the morbidity and mortality associated with cigarette use. Next-generation products (NGPs), as alternatives to combustible cigarettes, such as electronic cigarettes (e-cig) and tobacco heating products (THPs), have been proposed as a harm reduction strategy to reduce the deleterious impacts of cigarette smoking. In this review, we examine the impact of tobacco smoke and MRPs on oxidative stress in different pathologies, including respiratory and cardiovascular diseases and tumors. The impact of tobacco cigarette smoke on oxidative stress signaling in human health is well established, whereas the safety profile of MRPs seems to be higher than tobacco cigarettes, but further, well-conceived, studies are needed to better understand the oxidative effects of these products with long-term exposure. Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
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