Increased chemokines levels in patients with chronic obstructive pulmonary disease: correlation with quantitative computed tomography metrics

Hao, Wendong; Li, Manxiang; Pang, Yamei; Du, Wenfeng; Huang, Xiaoqi

doi:10.1259/bjr.20201030

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…Overexpression of IL-18 in the airways in patients with COPD has been shown and can lead to emphysema, the development of fibrosis in the bronchi and blood vessels of the lungs, and the formation of pulmonary hypertension [7,8]. Due to its T-helper type 2 cell-(Th-2-) inducing functions, IL-18 can also participate in inflammation and hyperreactivity of the respiratory tract in asthma and promote the recruitment of eosinophils to the airways [9][10][11][12]. On the other hand, IL-18 would further induce immune cells to produce a large amount of inflammatory factors to aggravate the disease [13,14].…”

Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-γ from NK Cells

Liu

2021

Computational and Mathematical Methods in Medicine

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Background. N-Acetylcysteine (NAC) had exerted antioxidation and anti-inflammation effects on chronic obstructive pulmonary disease (COPD) patients. However, its effect in regulating interleukin- (IL-) 18 was not fully understood. This study was designed to evaluate the specific mechanism of NAC regulating IL-18. Materials and Methods. A total of 112 COPD patients and 103 health individuals were recruited in the study. Cytokine level in patients’ serum was measured by enzyme-linked immunosorbent assay (ELISA). A COPD mouse model was established by administration of lipopolysaccharide (LPS) and cigarette smoke. The expression of cytokines was measured by ELISA and flow cytometry. Inflammasome-related protein was measured by Western blot. Result. NAC could effectively improve the immune status of COPD patients as well as the COPD mouse model by downregulating proinflammation and inflammation cytokines including IL-1β, interferon- (IFN-) γ, tumor necrosis factor- (TNF-) α, and IL-18. It also had the capability to suppress synthesis of IL-18 in macrophage to inhibit the secretion of IFN-γ from natural killer (NK) cells through influencing the inflammasome-related protein in macrophages. Conclusion. NAC could effectively inhibit the production of IL-18 by suppressing NLRP3 expression in macrophages to reduce the production of IFN-γ in NK cells.

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Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-γ from NK Cells

Liu

2021

Computational and Mathematical Methods in Medicine

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“…Studies have found that CXCL12 is significantly upregulated in the serum of COPD patients compared with that of healthy controls, and is positively correlated with small airway disease and emphysema detected using high-resolution chest CT scans. 51 When the Cxcl12/Cxcr4 signaling axis was blocked, the number of neutrophils decreased, and reverse migration increased inflammation levels. 52 The CXCL12 antagonist, AMD3100, can ameliorates emphysema-like manifestations in mice induced using cigarette smoke.…”

Section: Discussionmentioning

confidence: 99%

Identification of Hub Genes Associated with COPD Through Integrated Bioinformatics Analysis

Chen¹,

Zhu²,

Huang³

et al. 2022

COPD

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Smoking is recognized as a risk factor for Chronic Obstructive Pulmonary Disease (COPD), yet only 20-25% of smokers eventually develop COPD. Since its molecular pathogenesis remains unclear, there is an important need to further understand genetic differences between smokers with COPD and healthy smokers, screen out high-risk and susceptible groups among smokers, and find effective therapeutic targets. Methods: Bioinformatics tools were used to screen biomarkers that were significantly associated with COPD smokers and healthy smokers. qRT-PCR and Western blotting analysis were used to detect hub gene expression in CSE-treated BEAS-2B cells and lung tissue of COPD mouse models. Results: Our study identified 132 DEGs. The GO and KEGG analyses suggested that the ECM-receptor interaction, MAPK signaling pathway, Chemokine signaling pathway, PI3K-Akt signaling pathway, extracellular matrix organization and collagen fibril organization were associated with the occurrence and development of COPD. In addition, WGCNA analysis of GSE1650 showed that the brown module was most correlated with COPD. The intersection between the brown module and DEGs was used to identify 9 HUB genes (COL14A1, SULF1, MOXD1, CXCL12, CHRNA1, COMP, POU2AF1, MMP11, THBS2) that showed consistent expression and upregulation. Both the mRNA and protein expression levels of the Hub genes (except that of MMP11) were significantly upregulated in tobacco smoke exposed mouse emphysema models and CSE treated BEAS-2B cells. Conclusion:Our results suggest that COL14A1, SULF1, MOXD1, CXCL12, CHRNA1, COMP, POU2AF1, and THBS2 may be potentially useful biomarkers for identifying smokers with a risk of developing COPD. The GO and KEGG functional enrichment analyses further confirmed the significant role played by ECM in the pathogenesis of COPD. The results of this study may provide further insights into the pathogenetic mechanisms involved in COPD.

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“…Chemokines mediate recruitment of immune cells into inflammatory lesions, and are related to the development of COPD. 19 A previous study has demonstrated that CXCL10 could recruit CXCR3+ type-1 T-lymphocytes to the peripheral airways of smokers with COPD, and type-1 T-lymphocytes express interferon gamma to promote activation of macrophages, thus releasing inflammatory cytokines, including IL-6, IL-8, TNF-α, and IL-1β. (20) Therefore, increased serum CXCL10 was regarded as a biomarker of COPD.…”

Section: Competing Interestsmentioning

confidence: 99%

PRMT5 promotes inflammation of cigarette smoke extract-induced bronchial epithelial cells by up-regulation of CXCL10

2021

aei

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Background: Chronic obstructive pulmonary disease (COPD) is related to inflammation and obstruction of the lungs and airways. Protein arginine methyltransferase 5 (PRMT5) that pro-motes arginine methylation of histones is associated with inflammation of endothelial cell and is implicated in lung branching morphogenesis and progression of lung cancer. The mechanism of PRMT5 in inflammatory response of COPD was explored in this study.Methods: Human bronchial epithelial cells, 16HBE, were treated with cigarette smoke extract for 24 h to establish cell model of COPD. Cell viability was examined by MTT assay. Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays were used to explore expression of PRMT5. Expression of Interleukin (IL)-6, IL-8, tumor necrosis factor-α (TNF-α), and IL-1β were investigated by enzyme-linked-ithe mmunosorbent serologic assay.Results: Cigarette smoke extract treatment induced cytotoxity of 16HBE with reduced cell via-bility. PRMT5 was enhanced in cigarette smoke extract-induced 16HBE. Knockdown of PRMT5 increased cell viability of cigarette smoke extract-induced 16HBE, and attenuated cigarette smoke extract-induced increase of IL-6, IL-8, TNF-α, and IL-1β. Up-regulation of C-X-C Motif Chemokine 10 (CXCL10) in cigarette smoke extract-induced 16HBE was restored by knockdown of PRMT5. Over-expression of CXCL10 counteracted with the suppressive effect of PRMT5 silence on expression of IL-6, IL-8, TNF-α, and IL-1β. Moreover, PRMT5 silence-induced increase of cell viability in cigarette smoke extract-induced 16HBE was reversed by over-expression of CXCL10.Conclusion: Knockdown of PRMT5 promoted cell viability of cigarette smoke extract-induced 16HBE, and reduced inflammation through down-regulation of CXCL10.

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Increased chemokines levels in patients with chronic obstructive pulmonary disease: correlation with quantitative computed tomography metrics

Cited by 8 publications

References 33 publications

N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-γ from NK Cells

N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-γ from NK Cells

Identification of Hub Genes Associated with COPD Through Integrated Bioinformatics Analysis

PRMT5 promotes inflammation of cigarette smoke extract-induced bronchial epithelial cells by up-regulation of CXCL10

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