1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients

Yang, Haihua; Long, Feng; You-zhi, Zhang; Yu, Ronghuan; Zhang, Peng; Li, Wenjing; Li, Shuijun; Jin, Xian-qiao; Xia, Jie; Dong, Liang; Zhu, Ning; Huang, Ying; Gong, Yi; Chen, Xiao

doi:10.1371/journal.pone.0120515

Cited by 25 publications

(15 citation statements)

References 24 publications

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“…1,25 (OH) 2 D did not show any effect on the phagocytic capacity of these macrophages but it increased the levels of cathelicidin [36]. Furthermore, in venous blood samples, the rate of peripheral blood neutrophilic apoptosis in patients with acute exacerbations of COPD was slower than in healthy controls and this neutrophilic apoptosis is increased after administration of vitamin D through the p38MAPK pathway [91]. Taken together, even though in a controlled setting of cell culture, these data clearly show that vitamin D has potential to interfere with the immune reaction in response to a respiratory infection in COPD.…”

Section: Vitamin D In Copd and Exacerbationsmentioning

confidence: 84%

Targeting Vitamin D Deficiency to Limit Exacerbations in Respiratory Diseases: Utopia or Strategy With Potential?

et al. 2019

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Patients with respiratory diseases such as cystic fibrosis, chronic obstructive pulmonary disease, or asthma often experience an acute worsening of respiratory symptoms, termed exacerbations. Although the course of exacerbations is disease specific, they are mostly triggered by a respiratory infection. Exacerbations often require hospitalization and are an important cause of mortality. Treatments of exacerbations aim to minimize the negative impact and to prevent subsequent events. Despite many existing therapy options, many patients do not benefit from therapy and suffer from recurrent events. Vitamin D deficiency is a worldwide problem and is extremely prevalent in these patients. Vitamin D, known for its calcemic effects, also has immunomodulatory and anti-infectious actions and can therefore be a possible agent to treat or prevent exacerbations. This review will focus on vitamin D as a potential candidate to treat or prevent exacerbations in CF, COPD, and asthma.

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Section: Vitamin D In Copd and Exacerbationsmentioning

confidence: 84%

Targeting Vitamin D Deficiency to Limit Exacerbations in Respiratory Diseases: Utopia or Strategy With Potential?

et al. 2019

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“…When neutrophil has hyperactivity in metabolism due to various factors, the metabolites including ROS radical group rises and cause inflammatory injuries in airway and lung tissues [20,21]. In studies investigating the relationship between neutrophil apoptosis delay and pathogenesis of COPD, it was found that aberrant protein expression of apoptosis family is one of the key reasons for neutrophil apoptosis [22,23]. The CFTR chloride ion serves a critical role in apoptosis through regulating the levels of ROS and GSH [24,25].…”

Section: Discussionmentioning

confidence: 99%

Effect of lentivirus-mediated CFTR overexpression on oxidative stress injury and inflammatory response in the lung tissue of COPD mouse model

Yin

Fang

et al. 2020

Bioscience Reports

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We aimed to investigate the regulatory mechanism of lentivirus-mediated overexpression of cystic fibrosis transmembrane conductance regulator (CFTR) in oxidative stress injury and inflammatory response in the lung tissue of mouse model of chronic obstructive pulmonary disease (COPD). COPD mouse model induced by cigarette smoke was established and normal mice were used as control. The mice were assigned into a normal group (control), a model group (untreated), an oe-CFTR group (injection of lentivirus overexpressing CFTR), and an oe-NC group (negative control, injection of lentivirus expressing irrelevant sequences). Compared with the oe-NC group, the oe-CFTR group had higher CFTR expression and a better recovery of pulmonary function. CFTR overexpression could inhibit the pulmonary endothelial cell apoptosis, reduce the levels of glutathione (GSH), reactive oxygen species (ROS), and malondialdehyde (MDA) and increase the values of superoxide dismutase (SOD), GSH peroxidase (GSH-Px), and total antioxidant capacity (T-AOC). The overexpression also led to reductions in the white blood cell (WBC) count in alveolus pulmonis, the concentrations of C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor-α, and the protein expressions of NF-κB p65, ERK, JNK, p-EPK, and p-JNK related to MAPK/NF-κB p65 signaling pathway. In conclusion, CFTR overexpression can protect lung tissues from injuries caused by oxidative stress and inflammatory response in COPD mouse model. The mechanism behind this may be related to the suppression of MAPK/NF-κB p65 signaling pathway.

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“…Yang et al showed that the level of phospho-p38 MAPK was increased in peripheral blood neutrophils of acute exacerbation of COPD patients. 40 Li et al demonstrated that the ERK/p38 MAPK pathway was enhanced in CSE-induced HBE cells. 41 Li et al indicated that the phosphorylation of ERK and p38 was increased in mice exposed to cigarette smoke.…”

Section: Discussionmentioning

confidence: 99%

Annexin A1 is elevated in patients with COPD and affects lung fibroblast function

Lai¹,

Li²,

Mai³

et al. 2018

COPD

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PurposeFibrosis in peripheral airways is responsible for airflow limitation in chronic obstructive pulmonary disease (COPD). Annexin A1 modulates several key biological events during inflammation. However, little is known about its role in airway fibrosis in COPD. We investigated whether levels of Annexin A1 were upregulated in patients with COPD, and whether it promoted airway fibrosis.MethodsWe quantified serum Annexin A1 levels in never-smokers (n=12), smokers without COPD (n=11), and smokers with COPD (n=22). Correlations between Annexin A1 expression and clinical indicators (eg, lung function) were assessed. In vitro, human bronchial epithelial (HBE) cells were exposed to cigarette smoke extract (CSE) and Annexin A1 expression was assessed. Primary human lung fibroblasts were isolated from patients with COPD and effects of Annexin A1 on fibrotic deposition of lung fibroblasts were evaluated.ResultsSerum Annexin A1 was significantly higher in patients with Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines stage III or IV than in those with GOLD stages I or II (12.8±0.8 ng/mL versus 9.8±0.7 ng/mL; p=0.016). Annexin A1 expression was negatively associated with airflow obstruction (forced expiratory volume in one second % predicted; r=−0.72, p<0.001). In vitro, Annexin A1 was significantly increased in CSE-exposed HBE cells in a time- and concentration-dependent manner. Annexin A1 promoted lung fibroblasts proliferation, migration, differentiation, and collagen deposition via the ERK1/2 and p38 mitogen-activated protein kinase pathways.ConclusionAnnexin A1 expression is upregulated in patients with COPD and affects lung fibroblast function. However, more studies are needed to clarify the role of Annexin A1 in airway fibrosis of COPD.

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1α,25-Dihydroxyvitamin D3 Induces Neutrophil Apoptosis through the p38 MAPK Signaling Pathway in Chronic Obstructive Pulmonary Disease Patients

Cited by 25 publications

References 24 publications

Targeting Vitamin D Deficiency to Limit Exacerbations in Respiratory Diseases: Utopia or Strategy With Potential?

Targeting Vitamin D Deficiency to Limit Exacerbations in Respiratory Diseases: Utopia or Strategy With Potential?

Effect of lentivirus-mediated CFTR overexpression on oxidative stress injury and inflammatory response in the lung tissue of COPD mouse model

Annexin A1 is elevated in patients with COPD and affects lung fibroblast function

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