Oxidative Stress and Therapeutic Development in Lung Diseases

Villegas, Leah R.; Stidham, Timothy; Nozik‐Grayck, Eva

doi:10.4172/2161-105x.1000194

Cited by 48 publications

(24 citation statements)

References 159 publications

(116 reference statements)

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“…Cellular organelles such as mitochondria and peroxisomes are major sources of ROS and nitrogen species 9 . Production of reactive species by exogenous sources such as environmental toxins and diet promotes the onset of lung diseases 10 . The physical characteristics and the chemical composition of PM play a key role in ROS generation in vitro and in vivo [8][9][10] .…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Mechanisms of ultrafine particle-induced respiratory health effects

2020

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Particulate matter (PM) is the principal component of air pollution. PM includes a range of particle sizes, such as coarse, fine, and ultrafine particles. Particles that are <100 nm in diameter are defined as ultrafine particles (UFPs). UFPs are found to a large extent in urban air as both singlet and aggregated particles. UFPs are classified into two major categories based on their source. Typically, UFPs are incidentally generated in the environment, often as byproducts of fossil fuel combustion, condensation of semivolatile substances or industrial emissions, whereas nanoparticles are manufactured through controlled engineering processes. The primary exposure mechanism of PM is inhalation. Inhalation of PM exacerbates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain unclear. This review offers insights into the mechanisms by which particles, including UFPs, influence airway inflammation and discusses several mechanisms that may explain the relationship between particulate air pollutants and human health, particularly respiratory health. Understanding the mechanisms of PMmediated lung injury will enhance efforts to protect at-risk individuals from the harmful health effects of air pollutants.

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Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Mechanisms of ultrafine particle-induced respiratory health effects

2020

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“…Amongst targetted macromolecules, lipids are the most affected by oxidation and generate peroxidation products. This established oxidative/hyperoxic stress in turn generates a general inflammation status of the lung tissue [44,45]. In this context, the activation of genes that encodes for antioxidant/detoxifying enzymes seems to have a crucial role.…”

Section: Osmentioning

confidence: 99%

Role of the Nrf2/HO-1 axis in bronchopulmonary dysplasia and hyperoxic lung injuries

et al. 2017

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Bronchopulmonary dysplasia (BPD) is a chronic illness that usually originates in preterm newborns. Generally, BPD is a consequence of respiratory distress syndrome (RDS) which, in turn, comes from the early arrest of lung development and the lack of pulmonary surfactant. The need of oxygen therapy to overcome premature newborns' compromised respiratory function generates an increasing amount of reactive oxygen species (ROS), the onset of sustained oxidative stress (OS) status, and inflammation in the pulmonary alveoli deputies to respiratory exchanges. BPD is a severe and potentially life-threatening disorder that in the most serious cases, can open the way to neurodevelopmental delay. More importantly, there is no adequate intervention to hamper or treat BPD. This perspective article seeks to review the most recent and relevant literature describing the very early stages of BPD and hyperoxic lung injuries focussing on nuclear factor erythroid derived 2 (Nrf2)/heme oxygenase-1 (HO-1) axis. Indeed, Nrf2/HO1 activation in response to OS induced lung injury in preterm concurs to the induction of certain number of antioxidant, anti-inflammatory, and detoxification pathways that seem to be more powerful than the activation of one single antioxidant gene. These elicited protective effects are able to counteract/mitigate all multifaceted aspects of the disease and may support novel approaches for the management of BPD.

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“…Nitric oxide (NO) produced in large amounts by inducible nitric oxide synthase (iNOS) occurs mainly in macrophages inflammatory situations and causes lipid peroxidation and the generation of isoprostane (Villegas et al, 2014 ). The 8-isoprostane prostaglandin 2α (8-iso-PGF2α) is considered the predominant marker of tissue oxidative damage form generated during free radical attack of cell membranes (Elfsmark et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Anti-IL17 on Acute Lung Injury Induced by LPS in Mice

et al. 2018

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Introduction: T helper 17 (Th17) has been implicated in a variety of inflammatory lung and immune system diseases. However, little is known about the expression and biological role of IL-17 in acute lung injury (ALI). We investigated the mechanisms involved in the effect of anti-IL17 in a model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice.Methods: Mice were pre-treated with anti-IL17, 1h before saline/LPS intratracheal administration alongside non-treated controls and levels of exhaled nitric oxide (eNO), cytokine expression, extracellular matrix remodeling and oxidative stress, as well as immune cell counts in bronchoalveolar lavage fluid (BALF), and respiratory mechanics were assessed in lung tissue.Results: LPS instillation led to an increase in multiple cytokines, proteases, nuclear factor-κB, and Forkhead box P3 (FOXP3), eNO and regulators of the actomyosin cytoskeleton, the number of CD4+ and iNOS-positive cells as well as the number of neutrophils and macrophages in BALF, resistance and elastance of the respiratory system, ARG-1 gene expression, collagen fibers, and actin and 8-iso-PGF2α volume fractions. Pre-treatment with anti-IL17 led to a significant reduction in the level of all assessed factors.Conclusions: Anti-IL17 can protect the lungs from the inflammatory effects of LPS-induced ALI, primarily mediated by the reduced expression of cytokines and oxidative stress. This suggests that further studies using anti-IL17 in a treatment regime would be highly worthwhile.

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Oxidative Stress and Therapeutic Development in Lung Diseases

Cited by 48 publications

References 159 publications

Mechanisms of ultrafine particle-induced respiratory health effects

Mechanisms of ultrafine particle-induced respiratory health effects

Role of the Nrf2/HO-1 axis in bronchopulmonary dysplasia and hyperoxic lung injuries

Protective Effects of Anti-IL17 on Acute Lung Injury Induced by LPS in Mice

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