Chronic Obstructive Pulmonary Disease

Duffy, Sean; Criner, Gerard J.

doi:10.1016/j.mcna.2018.12.005

Cited by 122 publications

(83 citation statements)

References 36 publications

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“…We investigated the concentration of serum IL-32 in stable COPD patients and found that the serum concentration of IL-32 in patients with stable COPD was higher than that in healthy individuals, indicating that there was a correlation between increased serum concentration of IL-32 and COPD. Previous studies show that IL-32 can activate the phosphorylation of the nuclear transcription factor kappa B (NF-κB) and p38 mitogen-activated protein kinase (p38MAPK), inducing the production of inflammatory factors such as tumor necrosis factor-α (TNF-α), IL-1β, IL-6 and IL-8, these cytokines play an important role in the pathogenesis of COPD 10,14 .…”

Section: Discussionmentioning

confidence: 99%

Correlation between serum IL-32 concentration and clinical parameters of stable COPD: a retrospective clinical analysis

Biaoxue

Fu²,

Rong³

et al. 2020

Sci Rep

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This study was to investigate the association between serum interleukin 32 (IL-32) concentration and clinical parameters in patients with stable chronic obstructive pulmonary disease (COPD). One hundred and sixteen patients with stable COPD and 70 healthy subjects were included in the study. The serum concentration of IL-32 was detected by enzyme-linked immunosorbent assay. The correlation between serum IL-32 and clinical parameters of patients with COPD was analyzed by T-test, one-way analysis of variance, multiple linear regression and receiver operating characteristic curve. The serum concentration of IL-32 in patients with stable COPD was higher than that in healthy control group (p < 0.001) and increased serum IL-32 was positively correlated with GOLD grading (p = 0.026), mMRC score (p = 0.004) and clinical medical history (p = 0.005), but negatively related to FEV1/FVC (p = 0.001) and FEV1% predicted (p = 0.001). Patient's COPD grading (p = 0.001), clinical medical history (p < 0.001) and FEV1/FVC (p = 0.001) exerted a significant impact on serum IL-32. The sensitivity and specificity of serum IL-32 for discerning COPD patients from healthy individuals were 85.34% and 64.29%, and the area under the curve was 0.808 (p < 0.001). Increased IL-32 is involved in the chronic disease progression of COPD, suggesting that IL-32 may be a molecular biomarker that reflects the severity of COPD and contributes to the disease diagnosis. Abbreviations BMI Body mass index CI Confidence interval COPD Chronic obstructive pulmonary disease FEV1 The value of forced expiratory volume in one second FVC Forced vital capacity GOLD The Global Initiative for Chronic Obstructive Pulmonary Disease ICAM Cell adhesion factor IL

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Section: Discussionmentioning

confidence: 99%

Correlation between serum IL-32 concentration and clinical parameters of stable COPD: a retrospective clinical analysis

Biaoxue

Fu²,

Rong³

et al. 2020

Sci Rep

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“…Pulmonary inflammation, oxidative stress, protease and anti-protease imbalance play important roles in the pathogenesis of COPD 3 . Inflammatory cells, epithelial cells and other structural cells release a variety of inflammatory mediators, attract circulating inflammatory cells, amplify the inflammatory process, and induce changes in lung tissue structure 4 , 5 . Studies suggest that chronic airway inflammation in COPD involves multiple cytokines, which causes high secretion of mucus and obstruction of small airways, as well as damage to the lung parenchyma, and thus resulting in restricted airflow and excessive lung inflation 3 – 6 .…”

Section: Introductionmentioning

confidence: 99%

“…Chemokine (C–C motif) ligand 18 (CCL18) is a polypeptide composed of 69 amino acids with a molecular weight of 7.85 KDa, it is secreted protein that belongs to the intercrine beta (chemokine CC) family 4 . It is reported that CCL18 is highly expressed in the lung, lymph nodes, placenta, bone marrow, and dendritic cells, it is a chemotactic factor that attracts lymphocytes but not monocytes or granulocytes 7 .…”

Section: Introductionmentioning

confidence: 99%

Association between serum CCL-18 and IL-23 concentrations and disease progression of chronic obstructive pulmonary disease

Biaoxue

Fu²,

Rong³

et al. 2020

Sci Rep

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This study aimed to investigate the association between serum concentrations of chemokine (C–C Motif) ligand 18 (CCL-18) and interleukin 23 (IL-23) and clinical parameters of chronic obstructive pulmonary disease (COPD). The serum concentrations of CCL-18 and IL-23 were tested by enzyme linked immunosorbent assay (ELISA). The association between their concentrations and clinical parameters of COPD patients were analyzed by linear regression, logistic regression and ROC curve. The results showed that the serum concentrations of CCL-18 and IL-23 in COPD patients were increased compared with healthy people (P < 0.001) and that patients with acute exacerbation of COPD (AECOPD) had higher serum CCL-18 and IL-23 concentrations than stable patients (P < 0.001). Synergistic increase of CCL-18 and IL-23 in COPD patients was positively correlated with COPD patients' higher GOLD grade (P < 0.001), higher mMRC score (P < 0.001) and longer medical history (P < 0.001), but negatively correlated with the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) (P < 0.001) and FEV1% predicted (P < 0.001). The serum concentrations of CCL-18 and IL-23 were most related to the GOLD grade (OR = 2.764 for CCL-18 and OR = 4.215 for IL-23) and detection of both showed considerable sensitivity (72.57% for CCL-18 and 76.92% for IL-23) and specificity (92.50% for CCL-18 and 77.5% for IL-23) in identifying COPD. Increased serum concentrations of CCL-18 and IL-23 correlated with the disease progression of COPD and they could be used as biomarkers for disease evaluation of COPD.

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“…Cigarette smoking is the main cause of COPD globally, moreover, exposure to smoke and particles from biomass fuel may become more important than cigarette smoke [4]. COPD is an often-progressive in ammatory disease of the airways caused by cigarette smoke.…”

Section: Introductionmentioning

confidence: 99%

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

Zhang¹,

Wang²,

Liu³

et al. 2020

Preprint

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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Chronic Obstructive Pulmonary Disease

Cited by 122 publications

References 36 publications

Correlation between serum IL-32 concentration and clinical parameters of stable COPD: a retrospective clinical analysis

Correlation between serum IL-32 concentration and clinical parameters of stable COPD: a retrospective clinical analysis

Association between serum CCL-18 and IL-23 concentrations and disease progression of chronic obstructive pulmonary disease

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

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