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Antioxidants
Special Issues
Airway Inflammation Induced by Oxidative Stress
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Airway Inflammation Induced by Oxidative Stress

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 (10 January 2023) | Viewed by 25785

Special Issue Editor

Dr. Samuel Santos Valença

E-Mail Website
Guest Editor
Instituto de Ciências Biomedicas, Universidade Federal do Rio Janeiro, Rio de Janeiro 21941-590, RJ, Brazil
Interests: redox biology and inflammation related to acute and chronic lung diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress has been described as a biochemical phenomenon caused by an imbalance between production and accumulation of oxidants in cells and tissue rather than the ability of a biological system to detoxify these reactive products. Reactive oxygen and nitrogen species, the most common oxidants, have been implicated in the pathogenesis of numerous disease processes. There are several events related to oxidative stress, which are important in the pathogenesis of lung diseases. These include oxidative inactivation of antiproteinases, airspace epithelial injury, increased sequestration of leukocytes in the pulmonary microvasculature, and gene expression of proinflammatory mediators. Epithelial cells in the lungs are uniquely vulnerable to oxidative damage due to their potential for exposure to both endogenous and exogenous oxidants. Lung cells use several nonenzymatic and enzymatic antioxidant mechanisms to protect against oxidative insult through redox-sensitive transcription factors such as Nrf2, NF-kB and AP-1, which regulate genes for proinflammatory mediators and protective mechanisms, such as antioxidant gene expression. Although antioxidant drugs could play a useful role in the therapy of inflammatory lung diseases, their clinical impact is relatively modest at present.

This Special Issue of Antioxidants aims to publish manuscripts that will explore all aspects of airway inflammation induced by oxidative stress by focusing on the pathophysiology mechanism of several stimuli and lung diseases. Original papers describing recent discoveries in the field of lung redox biology and inflammation are welcome, as well as reviews from experts in this field.

Prof. Dr. Samuel Santos Valença
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

  • lung injury
  • inflammation
  • oxidative stress
  • biomarkers

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Published Papers (7 papers)

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Research

Jump to: Review

22 pages, 1269 KiB  
Article
Effects of Hyperoxia and Hyperoxic Oscillations on the Proteome of Murine Lung Microvascular Endothelium
by Akos Tiboldi, Eva Hunyadi-Gulyas, Peter Wohlrab, Johannes A. Schmid, Klaus Markstaller, Klaus Ulrich Klein and Verena Tretter
Antioxidants 2022, 11(12), 2349; https://doi.org/10.3390/antiox11122349 - 28 Nov 2022
Cited by 1 | Viewed by 1864
Abstract
Patients presenting with insufficient tissue oxygenation and impaired lung function as in acute respiratory distress syndrome (ARDS) frequently require mechanical ventilation with supplemental oxygen. Despite the lung being used to experiencing the highest partial pressure of oxygen during healthy breathing, the organ is [...] Read more.
Patients presenting with insufficient tissue oxygenation and impaired lung function as in acute respiratory distress syndrome (ARDS) frequently require mechanical ventilation with supplemental oxygen. Despite the lung being used to experiencing the highest partial pressure of oxygen during healthy breathing, the organ is susceptible to oxygen-induced injury at supraphysiological concentrations. Hyperoxia-induced lung injury (HALI) has been regarded as a second hit to pre-existing lung injury and ventilator-induced lung injury (VILI) attributed to oxidative stress. The injured lung has a tendency to form atelectasis, a cyclic collapse and reopening of alveoli. The affected lung areas experience oxygen conditions that oscillate between hyperoxia and hypoxia rather than remaining in a constant hyperoxic state. Mechanisms of HALI have been investigated in many animal models previously. These studies provided insights into the effects of hyperoxia on the whole organism. However, cell type-specific responses have not been dissected in detail, but are necessary for a complete mechanistic understanding of ongoing pathological processes. In our study, we investigated the effects of constant and intermittent hyperoxia on the lung endothelium from a mouse by an in vitro proteomic approach. We demonstrate that these oxygen conditions have characteristic effects on the pulmonary endothelial proteome that underlie the physiological (patho)mechanisms. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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23 pages, 4762 KiB  
Article
Cigarette Smoke Impairs Airway Epithelial Wound Repair: Role of Modulation of Epithelial-Mesenchymal Transition Processes and Notch-1 Signaling
by Serena Di Vincenzo, Dennis K. Ninaber, Chiara Cipollina, Maria Ferraro, Pieter S. Hiemstra and Elisabetta Pace
Antioxidants 2022, 11(10), 2018; https://doi.org/10.3390/antiox11102018 - 12 Oct 2022
Cited by 9 | Viewed by 2097
Abstract
Cigarette smoke (CS) induces oxidative stress and chronic inflammation in airway epithelium. It is a major risk factor for respiratory diseases, characterized by epithelial injury. The impact of CS on airway epithelial repair, which involves epithelial-mesenchymal transition (EMT) and the Notch-1 pathway, is [...] Read more.
Cigarette smoke (CS) induces oxidative stress and chronic inflammation in airway epithelium. It is a major risk factor for respiratory diseases, characterized by epithelial injury. The impact of CS on airway epithelial repair, which involves epithelial-mesenchymal transition (EMT) and the Notch-1 pathway, is incompletely understood. In this study, we used primary bronchial epithelial cells (PBECs) to evaluate the effect of CS on epithelial repair and these mechanisms. The effect of CS and/or TGF-beta1 on wound repair, various EMT and Notch-1 pathway markers and epithelial cell markers (TP63, SCGB1A) was assessed in PBECs cultured submerged, at the air–liquid interface (ALI) alone and in co-culture with fibroblasts. TGF-beta1 increased epithelial wound repair, activated EMT (shown by decrease in E-cadherin, and increases in vimentin, SNAIL1/SNAIL2/ZEB1), and increased Notch-1 pathway markers (NOTCH1/JAGGED1/HES1), MMP9, TP63, SCGB1A1. In contrast, CS decreased wound repair and vimentin, NOTCH1/JAGGED1/HES1, MMP9, TP63, SCGB1A1, whereas it activated the initial steps of the EMT (decrease in E-cadherin and increases in SNAIL1/SNAIL2/ZEB1). Using combined exposures, we observed that CS counteracted the effects of TGF-beta1. Furthermore, Notch signaling inhibition decreased wound repair. These data suggest that CS inhibits the physiological epithelial wound repair by interfering with the normal EMT process and the Notch-1 pathway. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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21 pages, 8098 KiB  
Article
Gold Nanoparticles Inhibit Steroid-Insensitive Asthma in Mice Preserving Histone Deacetylase 2 and NRF2 Pathways
by Magda F. Serra, Amanda C. Cotias, Andreza S. Pimentel, Ana Carolina S. de Arantes, Ana Lucia A. Pires, Manuella Lanzetti, Jandir M. Hickmann, Emiliano Barreto, Vinicius F. Carvalho, Patrícia M. R. e Silva, Renato S. B. Cordeiro and Marco Aurélio Martins
Antioxidants 2022, 11(9), 1659; https://doi.org/10.3390/antiox11091659 - 26 Aug 2022
Cited by 8 | Viewed by 2054
Abstract
Background: Gold nanoparticles (AuNPs) can inhibit pivotal pathological changes in experimental asthma, but their effect on steroid-insensitive asthma is unclear. The current study assessed the effectiveness of nebulized AuNPs in a murine model of glucocorticoid (GC)-resistant asthma. Methods: A/J mice were sensitized and [...] Read more.
Background: Gold nanoparticles (AuNPs) can inhibit pivotal pathological changes in experimental asthma, but their effect on steroid-insensitive asthma is unclear. The current study assessed the effectiveness of nebulized AuNPs in a murine model of glucocorticoid (GC)-resistant asthma. Methods: A/J mice were sensitized and subjected to intranasal instillations of ovalbumin (OVA) once a week for nine weeks. Two weeks after starting allergen stimulations, mice were subjected to Budesonide or AuNP nebulization 1 h before stimuli. Analyses were carried out 24 h after the last provocation. Results: We found that mice challenged with OVA had airway hyperreactivity, eosinophil, and neutrophil infiltrates in the lung, concomitantly with peribronchiolar fibrosis, mucus production, and pro-inflammatory cytokine generation compared to sham-challenged mice. These changes were inhibited in mice treated with AuNPs, but not Budesonide. In the GC-resistant asthmatic mice, oxidative stress was established, marked by a reduction in nuclear factor erythroid 2-related factor 2 (NRF2) levels and catalase activity, accompanied by elevated values of thiobarbituric acid reactive substances (TBARS), phosphoinositide 3-kinases δ (PI3Kδ) expression, as well as a reduction in the nuclear expression of histone deacetylase 2 (HDAC2) in the lung tissue, all of which sensitive to AuNPs but not Budesonide treatment. Conclusion: These findings suggest that AuNPs can improve GC-insensitive asthma by preserving HDAC2 and NRF2. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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18 pages, 3865 KiB  
Article
Treatment with Bixin-Loaded Polymeric Nanoparticles Prevents Cigarette Smoke-Induced Acute Lung Inflammation and Oxidative Stress in Mice
by Alexsandro Tavares Figueiredo-Junior, Samuel Santos Valença, Priscilla Vanessa Finotelli, Francisca de Fátima dos Anjos, Lycia de Brito-Gitirana, Christina Maeda Takiya and Manuella Lanzetti
Antioxidants 2022, 11(7), 1293; https://doi.org/10.3390/antiox11071293 - 29 Jun 2022
Cited by 6 | Viewed by 1970
Abstract
The use of annatto pigments has been evaluated as a therapeutic strategy in animal models of several health disorders. Beneficial effects were generally attributed to the inhibition of oxidative stress. Bixin is the main pigment present in annatto seeds and has emerged as [...] Read more.
The use of annatto pigments has been evaluated as a therapeutic strategy in animal models of several health disorders. Beneficial effects were generally attributed to the inhibition of oxidative stress. Bixin is the main pigment present in annatto seeds and has emerged as an important scavenger of reactive oxygen (ROS) and nitrogen species (RNS). However, this carotenoid is highly hydrophobic, affecting its therapeutic applicability. Therefore, bixin represents an attractive target for nanotechnology to improve its pharmacokinetic parameters. In this study, we prepared bixin nanoparticles (npBX) and evaluated if they could prevent pulmonary inflammation and oxidative stress induced by cigarette smoke (CS). C57BL/6 mice were exposed to CS and treated daily (by gavage) with different concentrations of npBX (6, 12 and 18%) or blank nanoparticles (npBL, 18%). The negative control group was sham smoked and received 18% npBL. On day 6, the animals were euthanized, and bronchoalveolar lavage fluid (BALF), as well as lungs, were collected for analysis. CS exposure led to an increase in ROS and nitrite production, which was absent in animals treated with npBX. In addition, npBX treatment significantly reduced leukocyte numbers and TNF-α levels in the BALF of CS-exposed mice, and it strongly inhibited CS-induced increases in MDA and PNK in lung homogenates. Interestingly, npBX protective effects against oxidative stress seemed not to act via Nrf2 activation in the CS + npBX 18% group. In conclusion, npBX prevented oxidative stress and acute lung inflammation in a murine model of CS-induced acute lung inflammation. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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15 pages, 18245 KiB  
Article
Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
by Mun-Ock Kim, Jae-Won Lee, Jae Kyoung Lee, Yu Na Song, Eun Sol Oh, Hyunju Ro, Dahye Yoon, Yun-Hwa Jeong, Ji-Yoon Park, Sung-Tae Hong, Hyung Won Ryu, Su Ui Lee and Dae Young Lee
Antioxidants 2022, 11(4), 679; https://doi.org/10.3390/antiox11040679 - 30 Mar 2022
Cited by 9 | Viewed by 3385
Abstract
Cigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruction, and airway mucus hypersecretion. Although studies have shown that Korean black ginseng extract (BGE) has potent anti-inflammatory and antioxidant activities, the CS-induced inflammatory responses and molecular mechanisms are yet [...] Read more.
Cigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruction, and airway mucus hypersecretion. Although studies have shown that Korean black ginseng extract (BGE) has potent anti-inflammatory and antioxidant activities, the CS-induced inflammatory responses and molecular mechanisms are yet to be examined. The aim of this study was to examine the effect of BGE on the airway inflammatory response and its molecular mechanisms, using CS/lipopolysaccharides (LPS)-exposed animals and PMA-stimulated human airway epithelial NCI-H292 cells. The results show that BGE inhibited the recruitment of immune cells and the release of inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, elastase, and reactive oxygen species (ROS) in the airways of CS/LPS-exposed animals. BGE inhibited mucus secretion and the expression of Mucin 5AC (MUC5AC). Furthermore, BGE exhibited an anti-inflammatory effect by downregulating a signaling pathway mediated by transforming growth factor-β-activated kinase (TAK) 1, an important protein that accelerates inflammation by cigarette smoke (CS). Overall, the findings show that BGE inhibits lung inflammation and mucus secretion by decreasing the activation of TAK1 both in human epithelial cells and in CS/LPS-exposed animals, and could be a potential adjuvant in the treatment and prevention of airway inflammatory diseases caused by airway irritants such as CS. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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Review

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46 pages, 3961 KiB  
Review
Oxidative Stress and Inflammation in Acute and Chronic Lung Injuries
by Frank Silva Bezerra, Manuella Lanzetti, Renata Tiscoski Nesi, Akinori Cardozo Nagato, Cyntia Pecli e Silva, Emanuel Kennedy-Feitosa, Adriana Correa Melo, Isabella Cattani-Cavalieri, Luís Cristóvão Porto and Samuel Santos Valenca
Antioxidants 2023, 12(3), 548; https://doi.org/10.3390/antiox12030548 - 21 Feb 2023
Cited by 49 | Viewed by 7484
Abstract
Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, [...] Read more.
Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, currently available therapies primarily focus on alleviating disease symptoms rather than reversing and/or preventing lung pathology. Moreover, some supportive interventions, such as oxygen and mechanical ventilation, can lead to (further) deterioration of lung function and even the development of permanent injuries. Lastly, sepsis, which can originate extrapulmonary or in the respiratory system itself, contributes to many cases of lung-associated deaths. Considering these challenges, we aim to summarize molecular and cellular mechanisms, with a particular focus on airway inflammation and oxidative stress that lead to the characteristic pathophysiology of acute and chronic lung injuries. In addition, we will highlight the limitations of current therapeutic strategies and explore new antioxidant-based drug options that could potentially be effective in managing acute and chronic lung injuries. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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21 pages, 2989 KiB  
Review
Airway Smooth Muscle Regulated by Oxidative Stress in COPD
by Hiroaki Kume, Ryuki Yamada, Yuki Sato and Ryuichi Togawa
Antioxidants 2023, 12(1), 142; https://doi.org/10.3390/antiox12010142 - 6 Jan 2023
Cited by 16 | Viewed by 5734
Abstract
Since COPD is a heterogeneous disease, a specific anti-inflammatory therapy for this disease has not been established yet. Oxidative stress is recognized as a major predisposing factor to COPD related inflammatory responses, resulting in pathological features of small airway fibrosis and emphysema. However, [...] Read more.
Since COPD is a heterogeneous disease, a specific anti-inflammatory therapy for this disease has not been established yet. Oxidative stress is recognized as a major predisposing factor to COPD related inflammatory responses, resulting in pathological features of small airway fibrosis and emphysema. However, little is known about effects of oxidative stress on airway smooth muscle. Cigarette smoke increases intracellular Ca2+ concentration and enhances response to muscarinic agonists in human airway smooth muscle. Cigarette smoke also enhances proliferation of these cells with altered mitochondrial protein. Hydrogen peroxide and 8-isoprostans are increased in the exhaled breath condensate in COPD. These endogenous oxidants cause contraction of tracheal smooth muscle with Ca2+ dynamics through Ca2+ channels and with Ca2+ sensitization through Rho-kinase. TNF-α and growth factors potentiate proliferation of these cells by synthesis of ROS. Oxidative stress can alter the function of airway smooth muscle through Ca2+ signaling. These phenotype changes are associated with manifestations (dyspnea, wheezing) and pathophysiology (airflow limitation, airway remodeling, airway hyperresponsiveness). Therefore, airway smooth muscle is a therapeutic target against COPD; oxidative stress should be included in treatable traits for COPD to advance precision medicine. Research into Ca2+ signaling related to ROS may contribute to the development of a novel agent for COPD. Full article
(This article belongs to the Special Issue Airway Inflammation Induced by Oxidative Stress)
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