Relation of oxidant-antioxidant imbalance with disease progression in patients with asthma

Ahmad, Asrar; Shameem, Mohammad; Husain, Qayyum

doi:10.4103/1817-1737.102182

Cited by 90 publications

(36 citation statements)

References 48 publications

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“…It was also observed that resting or stimulated phagocytes may produce differently reactive oxygen species that depends on the disease form [27]. Predominance of enhancement of ROS has been observed in asthma [25-27]. The differences between our observations and other researchers who have assessed ROS in asthma are most likely the result of the type of ROS evaluated, the cell type assessed and differences in the clinical form and severity of the disease.…”

Section: Discussionmentioning

confidence: 40%

Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children

Silva-Martins

Couto²,

Muniz‐Junqueira³

2013

Clinical & Translational All

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BackgroundCorticosteroids are the first-line therapy for asthma; however, the effect of corticosteroids on the innate immune system remains unclear. This study’s objective was to evaluate the effect of inhaled corticosteroid therapy (ICT) on phagocytic functions.MethodsTo evaluate the impact of ICT, the phagocytosis of Saccharomyces cerevisiae by blood monocytes and neutrophils and the production of superoxide anions were assessed before and after three and six months of ICT treatment in 58 children with persistent asthma and 21 healthy controls.ResultsWe showed that the phagocytic capacity of monocytes and neutrophils that occurred via pattern recognition receptors or was mediated by complement and immunoglobulin receptors in asthmatic children before treatment was significantly lower than in healthy controls (p<0.05, Mann–Whitney test) and was not influenced by the severity of the clinical form of the disease. Although there was clinical improvement with treatment, ICT for 6 months was not sufficient to normalize phagocytosis by the phagocytes. Superoxide anion production was also decreased in the asthmatic children before treatment, and ICT normalized the O- production only for children with mild persistent asthma when assessed at baseline but caused this function to decrease after stimulation (p<0.05, Kruskal-Wallis test).ConclusionsOur data suggest that an immunodeficiency in phagocytes remained even after treatment. However, this immunodeficiency does not appear to correspond with the clinical evolution of asthma because an improvement in clinical parameters occurred.

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Section: Discussionmentioning

confidence: 40%

Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children

Silva-Martins

Couto²,

Muniz‐Junqueira³

2013

Clinical & Translational All

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“…The activity of SOD is as an intracellular antioxidant enzyme. SOD activity in the asthmatic patients was lower than that in the healthy controls [14]. The mechanism of oxidative stress in asthma remains unclear.…”

Section: Discussionmentioning

confidence: 70%

25-Hydroxyvitamin D3-Deficiency Enhances Oxidative Stress and Corticosteroid Resistance in Severe Asthma Exacerbation

Luo

Yang

et al. 2014

PLoS ONE

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Oxidative stress plays a significant role in exacerbation of asthma. The role of vitamin D in oxidative stress and asthma exacerbation remains unclear. We aimed to determine the relationship between vitamin D status and oxidative stress in asthma exacerbation. Severe asthma exacerbation patients with 25-hydroxyvitamin D3-deficiency (V-D deficiency) or 25-hydroxyvitamin D-sufficiency (V-D sufficiency) were enrolled. Severe asthma exacerbation with V-D-deficiency showed lower forced expiratory volume in one second (FEV1) compared to that with V-D-sufficiency. V-D-deficiency intensified ROS release and DNA damage and increased TNF-α, OGG1 and NFκB expression and NFκB phosphorylation in severe asthma exacerbation. Supplemental vitamin D3 significantly increased the rates of FEV1 change and decreased ROS and DNA damage in V-D-deficiency. Vitamin D3 inhibited LPS-induced ROS and DNA damage and were associated with a decline in TNF-α and NFκB in epithelial cells. H2O2 reduces nuclear translocation of glucocorticoid receptors in airway epithelial cell lines. V-D pretreatment enhanced the dexamethasone-induced nuclear translocation of glucocorticoid receptors in airway epithelial cell lines and monocytes from 25-hydroxyvitamin D3-deficiency asthma patients. These findings indicate that V-D deficiency aggravates oxidative stress and DNA damage, suggesting a possible mechanism for corticosteroid resistance in severe asthma exacerbation.

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“…Exposure to air pollutants can lead to oxidative stress in the airways, and there is compelling evidence that asthmatic airways are deficient in antioxidant defenses 89 . Furthermore, the antioxidant capacity of the lungs is inversely related to asthma severity 90 . In addition to lower levels of superoxide dismutase and catalase, 89 it has been shown that goblet cells express the high-affinity sodium ascorbate cotransporter, which is involved in vitamin C uptake into cells, and that expression of sodium ascorbate cotransporters is inversely related to lung lining fluid vitamin C levels 91 .…”

Section: Dysregulation Of the Epithelial Barrier In Asthmatic Patientsmentioning

confidence: 99%

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

Loxham

Davies

2017

Journal of Allergy and Clinical Immunology

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The bronchial epithelium is continuously exposed to a multitude of noxious challenges in inhaled air. Cellular contact with most damaging agents is reduced by the action of the mucociliary apparatus and by formation of a physical barrier that controls passage of ions and macromolecules. In conjunction with these defensive barrier functions, immunomodulatory cross-talk between the bronchial epithelium and tissue-resident immune cells controls the tissue microenvironment and barrier homeostasis. This is achieved by expression of an array of sensors that detect a wide variety of viral, bacterial, and nonmicrobial (toxins and irritants) agents, resulting in production of many different soluble and cell-surface molecules that signal to cells of the immune system. The ability of the bronchial epithelium to control the balance of inhibitory and activating signals is essential for orchestrating appropriate inflammatory and immune responses and for temporally modulating these responses to limit tissue injury and control the resolution of inflammation during tissue repair. In asthmatic patients abnormalities in many aspects of epithelial barrier function have been identified. We postulate that such abnormalities play a causal role in immune dysregulation in the airways by translating gene-environment interactions that underpin disease pathogenesis and exacerbation.

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Relation of oxidant-antioxidant imbalance with disease progression in patients with asthma

Cited by 90 publications

References 48 publications

Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children

Inhaled corticosteroid treatment for 6 months was not sufficient to normalize phagocytosis in asthmatic children

25-Hydroxyvitamin D3-Deficiency Enhances Oxidative Stress and Corticosteroid Resistance in Severe Asthma Exacerbation

Phenotypic and genetic aspects of epithelial barrier function in asthmatic patients

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