The Contribution of Oxidative Stress and Inflamm-Aging in Human and Equine Asthma

Bullone, Michela; Lavoie, Jean‐Pierre

doi:10.3390/ijms18122612

Cited by 65 publications

(38 citation statements)

References 217 publications

(293 reference statements)

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“…Evidences have revealed the role of oxidative stress in the pathogenesis of asthma (Bullone and Lavoie, 2017;Kleniewska and Pawliczak, 2017). The ROS in asthma could come from resident cells or immune cells.…”

Section: Oxidative Stressmentioning

confidence: 99%

Potential Role of Cellular Senescence in Asthma

Wang

Yang

et al. 2020

Front. Cell Dev. Biol.

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Cellular senescence is a complicated process featured by irreversible cell cycle arrest and senescence-associated secreted phenotype (SASP), resulting in accumulation of senescent cells, and low-grade inflammation. Cellular senescence not only occurs during the natural aging of normal cells, but also can be accelerated by various pathological factors. Cumulative studies have shown the role of cellular senescence in the pathogenesis of chronic lung diseases including chronic obstructive pulmonary diseases (COPD) and idiopathic pulmonary fibrosis (IPF) by promoting airway inflammation and airway remodeling. Recently, great interest has been raised in the involvement of cellular senescence in asthma. Limited but valuable data has indicated accelerating cellular senescence in asthma. This review will compile current findings regarding the underlying relationship between cellular senescence and asthma, mainly through discussing the potential mechanisms of cellular senescence in asthma, the impact of senescent cells on the pathobiology of asthma, and the efficiency and feasibility of using anti-aging therapies in asthmatic patients.

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Section: Oxidative Stressmentioning

confidence: 99%

Potential Role of Cellular Senescence in Asthma

Wang

Yang

et al. 2020

Front. Cell Dev. Biol.

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“…There is no current correlation between inflamm‐aging and the development of chronic inflammatory airway diseases. However, based on the human phenotype, we believe it is biologically appropriate to use RAO as an equine model for late‐onset asthma, as recently reviewed …”

Section: Late‐onset Asthmamentioning

confidence: 99%

Equine asthma: Integrative biologic relevance of a recently proposed nomenclature

Bond

Léguillette

Richard

et al. 2018

Veterinary Internal Medicne

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The term “equine asthma” has been proposed as a unifying descriptor of inflammatory airway disease (IAD), recurrent airway obstruction (RAO), and summer pasture‐associated obstructive airway disease. Whilst the term will increase comprehensibility for both the lay and scientific communities, its biologic relevance must be compared and contrasted to asthma in human medicine, recognizing the limited availability of peer‐reviewed equine‐derived data, which are largely restricted to clinical signs, measures of airway obstruction and inflammation and response to therapy. Such limitations constrain meaningful comparisons with human asthma phenotypes. Suggested minimum inclusion criteria supporting the term asthma, as well as similarities and differences between IAD, RAO, and multiple human asthma phenotypes are discussed. Furthermore, differences between phenotype and severity are described, and typical features for equine asthma subcategories are proposed. Based on shared features, we conclude that mild/moderate (IAD) and severe (RAO) equine asthma are biologically appropriate models for both allergic and non‐allergic human asthma, with RAO (severe equine asthma) also being an appropriate model for late‐onset asthma. With the development of new biologic treatments in humans and the application of more targeted therapeutic approaches in the horse, it would appear appropriate to further investigate the allergic (Th‐2) and non‐allergic (non‐Th‐2) phenotypes of equine asthma. Further research is required to more fully determine the potential clinical utility of phenotype classification.

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“…Numerous studies have shown that oxidative stress plays an important role in the pathogenesis of asthma (6)(7)(8). When airway inflammation occurs, inflammatory mediators such as histamine and leukotriene are released.…”

Section: Introductionmentioning

confidence: 99%

Edaravone attenuates experimental asthma in mice through induction of HO‑1 and the Keap1/Nrf2 pathway

Pan

Feng

et al. 2019

Exp Ther Med

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Asthma is a chronic disease that threatens public health worldwide. Multiple studies have shown that oxidative stress plays an important role in the pathogenesis of asthma. Edaravone (Eda), a free radical scavenger, has been found to have a protective effect against lung injury due to its ability to eliminate reactive oxygen species. The present study aimed to investigate the effect of Eda on asthma and the mechanism underlying its actions. An experimental asthma model was induced in mice, before they were treated with different doses of Eda. Measurements of airway responsiveness to methacholine (Mch), cell counts and cytokine levels in bronchoalveolar lavage fluid (BALF) and of the oxidative products and antioxidant enzymes in lung tissue were taken in these asthma model mice and compared with control mice. Protein levels of kelch-like ECH-associated protein-1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) were determined in the lung tissue of normal mice and Nrf2 and HO-1-deficient mice subject to the asthma model to investigate the mechanisms underlying Eda action. The results indicated that Eda effectively reduced airway responsiveness to Mch. The total number of cells and the numbers of eosinophils, lymphocytes and neutrophils in BALF of asthma model mice were also significantly reduced by Eda treatment when compared with normal saline treatment. Eda treatment significantly alleviated perivascular edema, peribronchial inflammation and macrophage infiltration in the alveolar space and decreased the levels of inflammatory cytokines released in BALF compared with control. Eda also significantly reduced the levels of oxidative stress markers in BALF and restored the levels of antioxidative enzyme, superoxide dismutase, when compared with control. The Keap1/Nrf2 ratio was significantly decreased with Eda compared with control due to an increase in Nrf2 and a decrease in Keap1 expression. HO-1 expression was increased by Eda. The airway responsiveness of Nrf2-/mice or HO-1-/mice to Mch was significantly higher compared with normal mice treated with Eda. Taken together, the results of the present study show that Eda exerts anti-inflammatory and antioxidative effects, which suggests a potential use for Eda in reduction of asthma severity. The activated Keap1/Nrf2 pathway and HO-1 may be involved in the anti-asthmatic effect of Eda.

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The Contribution of Oxidative Stress and Inflamm-Aging in Human and Equine Asthma

Cited by 65 publications

References 217 publications

Potential Role of Cellular Senescence in Asthma

Potential Role of Cellular Senescence in Asthma

Equine asthma: Integrative biologic relevance of a recently proposed nomenclature

Edaravone attenuates experimental asthma in mice through induction of HO‑1 and the Keap1/Nrf2 pathway

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