Sustained Elevation of Systemic Oxidative Stress and Inflammation in Exacerbation and Remission of Asthma

Mak, Jcw; Ho, Stanley; Ho, Alice; Law, Barbara K. W.; Cheung, Amy; Ho, J. C.; Ip, Tsun Kwan Mary; Chan‐Yeung, Moira

doi:10.1155/2013/561831

Cited by 25 publications

(18 citation statements)

References 34 publications

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“…Children with asthma may experience nocturnal hypoxemia and hypoventilation [ 31 ]. In addition, inflammation and remodeling of the airway [ 32 ], oxidative stress [ 33 ], and systemic inflammation [ 34 , 35 , 36 ] are reported in asthma patients. Oxidative stress ensues in diverse forms, producing complex structural and functional changes that have implications on cerebral perfusion and permeability of the blood–brain barrier [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Sleep-Disordered Breathing in Children with Recurrent Wheeze/Asthma: A Single Centre Study

et al. 2017

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The relationship between asthma and sleep-disordered breathing is bidirectional due to common risk factors that promote airway inflammation. Obstructive sleep-disordered breathing and recurrent wheeze/asthma are conditions that involve the upper and the lower respiratory system, respectively. The aim of the present study was to investigate the sleep disordered breathing in children with recurrent wheeze/asthma. This was a retrospective study concerning children older than 2 years who underwent—between January 2014 and November 2016—an in-laboratory overnight polygraphic study. We match the children between those who do or do not have recurrent wheeze/asthma disease. We examined the clinical records of 137 children. We excluded eight patients because of neurological and genetic conditions. Children with recurrent wheeze/asthma (N = 28) were younger (p = 0.002) and leaner (p = 0.013) compared to non-affected children (N = 98). Children with wheeze/asthma and unaffected ones had a similar obstructive apnea-hypopnea index (p = 0.733) and oxygen desaturation index (p = 0.535). The logistic regression analysis, in which the condition of wheeze/asthma (yes/no) was a dependent variable, while demographic (age, sex, body mass index (BMI) Z-score) and polygraphic results during sleep (obstructive apnea-hypopnea index, central apnea index, peripheral oxygen saturation (SpO2), and snoring) were covariates, showed that children with wheeze/asthma had higher central apnea index (Exp(B) = 2.212; Wald 6.845; p = 0.009). In conclusion, children with recurrent wheeze/asthma showed an increased number of central sleep apneas than unaffected children. This finding may suggest a dysfunction of the breathing control in the central nervous system during sleep. Systemic or central inflammation could be the cause.

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Section: Discussionmentioning

confidence: 99%

Sleep-Disordered Breathing in Children with Recurrent Wheeze/Asthma: A Single Centre Study

et al. 2017

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“…For example, Teng and colleagues have shown concentrations of H 2 O 2 are elevated in exhaled breath condensate of asthmatics compared with controls, with concentrations increasing with asthma severity [15]. Mak and colleagues have reported elevated plasma concentrations of 8-isoprostane, a lipid peroxide marker of oxidative stress, during asthma exacerbations [16]. Indeed oxidative stress has been implicated in many of the key pathophysiological features of asthma, including airways hyper-responsiveness and mucus hypersecretion (reviewed by Zuo et al [17], and Li et al [18]).…”

Section: Introductionmentioning

confidence: 99%

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Pfeffer

Mann

et al. 2018

Preprint

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41 Background: Particulate matter (PM) pollutant exposure, which induces oxidative stress and 42 inflammation, and vitamin D insufficiency, which compromises immune regulation, are 43 detrimental in asthma. 55 versus asthmatic donor cultures. Vitamin D also differentially affected PM-stimulated GM-56 CSF, with suppression in healthy HBECs and enhancement in asthmatic cultures. Vitamin D 57 increased HBEC expression of the antioxidant pathway gene G6PD, increased the ratio of 58 reduced to oxidised glutathione, and in PM-stimulated cultures decreased the formation of 8-59 isoprostane. Pre-treatment with vitamin D decreased CXCL8 and further decreased IL-6 60 production in PM-stimulated cultures, an effect abrogated by inhibition of G6PD with DHEA, 61 supporting a role for this pathway in the anti-inflammatory actions of vitamin D. 62 Conclusions: In a study using HBECs from 18 donors, vitamin D enhanced HBEC 63 antioxidant responses and modulated the immune response to PM, suggesting that vitamin D 64 may protect the airways from pathological pollution-induced inflammation. prevalence, implying the importance of environmental factors in its aetiology [1]. Vitamin D 68 insufficiency/deficiency and ambient air pollution are two major environmental factors that 69 appear to influence the pathogenesis and stability of asthma [2] [3] [4] [5], as well as other 70 respiratory diseases [6] [7]. However there remains debate resulting from the heterogeneity 71 of findings relating to the effects of these environmental factors on airway pathology [5] [8] [9] 72 [10]. For example, European studies have shown heterogeneity between different cities in 73 the magnitude of the effects of pollution on health outcomes such as hospital admissions for 74 respiratory diseases [9] and asthma incidence [11], despite using standardised analyses. 75 Environment-environment interactions are a major possible explanation for inconsistent 76 results between different patient cohorts but have been little studied, particularly at the 77 mechanistic level. In a recent meta-analysis, latitude of study location influenced 78 associations between air pollutants and severe asthma exacerbations, and latitude is also 79 known to affect sunlight-derived vitamin D production, although this association is 80 complicated by other factors such as hours of daily skin exposure to sunlight [5]. In the 81 urban environment Rosser and colleagues have shown that vitamin D insufficient children, 82 but not those vitamin D sufficient, living close to major roads show an elevated risk of severe 83 asthma exacerbations [12], although the mechanisms by which vitamin D may protect 84 against pollution toxicity remain unclear and the interaction likely complex. 85 86 A growing body of research highlights the importance of epithelial immunology in 87 asthma [13]. Evidence shows that inhaled ambient particulate matter (PM) adversely affects 88 the bronchial epithelium through various mechanisms including the imposition of oxidative 89 stress, which stimulates redox sensi...

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“…Several factors have been considered to be associated with the pathogenesis of asthma, among which obesity has been considered as an independent risk factor ( 1 ). Accumulating evidence indicates that an imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses, favoring a more oxidative state, is present in asthma or obesity ( 2 , 3 ). For example, in patients with asthma or obesity, the elevation of oxidative stress and changes in antioxidant defenses have been reported ( 2 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating evidence indicates that an imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses, favoring a more oxidative state, is present in asthma or obesity ( 2 , 3 ). For example, in patients with asthma or obesity, the elevation of oxidative stress and changes in antioxidant defenses have been reported ( 2 , 4 ). However, the potential mechanism underlying the association between obesity and asthma remain to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Correlation between oxidative stress and the NF-κB signaling pathway in the pulmonary tissues of obese asthmatic mice

Liu

Lin

Zhao

et al. 2015

Molecular Medicine Reports

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The obesity-asthma phenotype is characterized by increased asthma severity and decreased glucocorticoid responsiveness. To date, the mechanism underlying the association between obesity and asthma remain to be fully elucidated. The present study investigated the correlation between oxidative stress and the nuclear factor (NF)-κB pathway in obese asthmatic mice. The animals were divided into the following groups: Control (n=8), comprising C57BL/6J mice without exposure to a high-fat diet; non-obese asthma group (n=8), comprising mice of a normal weight subjected to the induction of asthma; obese control group (n=8), comprising C57BL/6J mice subjected to a high-fat diet; and obese asthmatic group (n=8), comprising obese mice subject to the induction of asthma. The levels of the malondialdehyde (MDA) oxidant and glutathione (GSH) antioxidant in the lungs and bronchoalveolar lavage fluid (BALF) were measured using ELISA. The expression levels of inhibitory κB kinase-β (IKK-β) and the inhibitor of κBα (IκB-α) in the pulmonary tissues was determined using western blot analysis. An electrophoretic mobility shift assay was performed to determine the transcription activity of NF-κB. The levels of MDA in the BALF and lung tissues increased significantly in the two asthmatic groups, compared with the control groups (P<0.01). The asthmatic mice showed significantly lower concentrations of GSH in the BALF and lung tissues, compared with the control groups (P<0.01). In the asthmatic animals, the expression of IκB kinase (IKK)-β and activation of NF-κB were upregulated in the pulmonary tissues, compared with those in the control groups (P<0.01). The expression of IKK-β and transcriptional activity of NF-κB were significantly higher the in obese asthmatic mice, compared with the non-obese asthmatic mice (P<0.01). On examining the expression levels of IκB-α in the pulmonary tissues, a significant reduction was found in the asthmatic animals, compared with the controls (P<0.01). In addition, the level of IκB-α was significantly lower in the obese asthmatics, compared with the non-obese asthmatics (P<0.01). MDA was positively correlated with NF-κB in the obese asthmatic group (R=0.83; P<0.05) and non-obese asthmatic group (R=0.82; P<0.05). Oxidative stress was upregulated in the pulmonary tissues of the asthmatic mice. This upregulation was more marked in the obese asthmatic mice, and was positively correlated with activation of the NF-κB signaling pathway in the pulmonary tissues. The results in the present study indicated that higher oxidative stress and activation of the NF-κB signaling pathway were observed in the lung tissues of the obese asthmatics. Furthermore, a positive correlation was identified between oxidative stress and NF-κB.

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Sustained Elevation of Systemic Oxidative Stress and Inflammation in Exacerbation and Remission of Asthma

Cited by 25 publications

References 34 publications

Sleep-Disordered Breathing in Children with Recurrent Wheeze/Asthma: A Single Centre Study

Sleep-Disordered Breathing in Children with Recurrent Wheeze/Asthma: A Single Centre Study

Effects of vitamin D on inflammatory and oxidative stress responses of human bronchial epithelial cells exposed to particulate matter

Correlation between oxidative stress and the NF-κB signaling pathway in the pulmonary tissues of obese asthmatic mice

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