Differences in Airway Remodeling Between Asthma and Chronic Obstructive Pulmonary Disease

2004 ◽  
Vol 27 (1) ◽  
pp. 035-044 ◽  
Author(s):  
Kazutetsu Aoshiba ◽  
Atsushi Nagai
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals The role of airway remodeling in the pathogenesis and treatment of chronic obstructive pulmonary disease

2021 ◽  
Vol 8 (3) ◽  
pp. 96-102
Author(s):  
Nightingale Syabbalo
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Epithelial Cells ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Inflammatory Cells ◽  
Lymphoid Cells ◽  
Standards Of Care ◽  
Chronic Obstructive ◽  
Small Airways ◽  
Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is currently considered the third leading cause of death in the world. COPD represents an important public health challenge and a socio-economical problem that is preventable and treatable. The main cause of COPD is chronic inhalation of cigarette smoke, and other harmful constituents of air pollution, which cause epithelial injury, chronic inflammation and airway remodeling. Airway remodeling is most prominent in small airways. It is due to infiltration of the airways by inflammatory cells, such as neutrophils, eosinophils, macrophages, and immune cells, including CD8+ T-cells, Th1, Th17 lymphocytes, and innate lymphoid cells group 3. Fibroblasts, myofibroblasts, and airway smooth muscle (ASM) cells also contribute to airway remodeling by depositing extracellular matrix (ECM) proteins, which increase the thickness of the airway wall. Activated inflammatory cells, and structural cells secrete cytokines, chemokines, growth factors, and enzymes which propagate airway remodeling. Airway remodeling is an active process which leads to thickness of the reticular basement membrane, subepithelial fibrosis, peribronchiolar fibrosis, and ASM cells hyperplasia and hypertrophy. It is also accompanied by submucosal glands and goblet cells hypertrophy and mucus hypersecretion, and angiogenesis. Epithelial mesenchymal transmission (EMT) plays a key role in airway remodeling. In patients with COPD and smokers, cellular reprograming in epithelial cells leads to EMT, whereby epithelial cells assume a mesencymal phenotype. Additionally, COPD is associated with increased parasympathetic cholinergic activity, which leads to ASM cells hypercontractility, increased mucus secretion, and vasodilatation. Treatment of COPD is intricate because of the heterogeneous nature of the disease, which requires specific treatment of the pathophysiological pathways, such as airway inflammation, ASM cell hypercontractility, and parasympathetic cholinergic hyperreactivity. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2020 strategy report recommends personalized approach for the treatment of COPD. However, some patients with COPD are unresponsive to the standards of care. They may require a triple combination of LABA/LAMA/ICS. Single-inhaler triple therapy (SITT), such as fluticasone fuorate/vilanterol/umeclidinium has been shown to significantly improve symptoms and asthma control, reduce moderate and severe exacerbations, and to improve lung function.

scholarly journals Yijin-Tang Attenuates Cigarette Smoke and Lipopolysaccharide-Induced Chronic Obstructive Pulmonary Disease in Mice

2022 ◽  
Vol 2022 ◽  
pp. 1-12
Author(s):  
Jinhyung Rho ◽  
Chang-Seob Seo ◽  
Eun-Ju Hong ◽  
Eun Bok Baek ◽  
Eunhye Jung ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Transforming Growth Factor ◽  
Airway Remodeling ◽  
Interleukin 1 ◽  
Chronic Obstructive ◽  
Necrosis Factor Alpha ◽  
Obstructive Pulmonary Disease ◽  
Cell Counts

Background. Chronic obstructive pulmonary disease (COPD) refers to a lung disorder associated with symptoms of dyspnea, cough, and sputum production. Traditionally, Yijin-tang (YJT), a mixture of Pinellia ternate, Poria cocos, ginger, Chinese liquorice, and tangerine peel, has been prescribed for the treatment of respiratory system diseases caused by dampness phlegm. This experiment investigated the therapeutic effect of YJT in a mouse model of cigarette smoke (CS)- and lipopolysaccharide (LPS)-induced COPD. Methods. COPD was induced by exposing mice to CS for 1 hour per day for 8 weeks, with intranasal delivery of LPS on weeks 1, 3, 5, and 7. YJT was administered at doses of 100 and 200 mg/kg 1 hour before CS exposure for the last 4 weeks. Results. YJT significantly suppressed CS- and LPS-induced increases in inflammatory cell counts and reduced interleukin-1 beta (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) levels in bronchoalveolar lavage fluid (BALF) and lung tissue. In addition, YJT not only decreased airway wall thickness, average alveolar intercept, and lung fibrosis, but it also suppressed the expression of matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-B (TGF-β) and collagen deposition. Moreover, YJT suppressed phosphorylation of nuclear factor-kappa B (NF-κB) as well as expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). Conclusion. Collectively, our findings show that YJT attenuates respiratory inflammation and airway remodeling caused by CS and LPS exposure; therefore, therapeutic applications in COPD can be considered.

scholarly journals Protective effect of Palmijihwanghwan in a mouse model of cigarette smoke and lipopolysaccharide-induced chronic obstructive pulmonary disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Eun Bok Baek ◽  
Jin-hyung Rho ◽  
Eunhye Jung ◽  
Chang-Seob Seo ◽  
Jin-Hee Kim ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Mouse Model ◽  
Protective Effect ◽  
Pulmonary Disease ◽  
Cigarette Smoke ◽  
Transforming Growth Factor ◽  
Airway Remodeling ◽  
Interleukin 1 ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Abstract Background Palmijihwanghwan (PJH) is a traditional medicine and eight constituents derived from PJH possess anti-inflammatory activities. However, the scientific evidence for its potential as a therapeutic agent for inflammatory lung disease has not yet been studied. In this study, we examined the protective effect of PJH in a mouse model of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) with lipopolysaccharide (LPS). Methods Mice received CS exposure for 8 weeks and intranasal instillation of LPS on weeks 1, 3, 5 and 7. PJH (100 and 200 mg/kg) was administrated daily 1 h before CS treatment for the last 4 weeks. Results Compared with CS plus LPS-exposed mice, mice in the PJH-treated group showed significantly decreased inflammatory cells count and reduced inflammatory cytokines including interleukin-1 beta (IL-1β), IL-6 and tumor necrosis factor alpha (TNF-α) levels in broncho-alveolar lavage fluid (BALF) and lung tissue. PJH also suppressed the phosphorylation of nuclear factor kappa B (NF-κB) and extracellular signal-regulated kinase1/2 (ERK1/2) caused by CS plus LPS exposure. Furthermore, CS plus LPS induced increases in matrix metallopeptidase (MMP)-7, MMP-9, and transforming growth factor-β (TGF-β) expression and collagen deposition that were inhibited in PJH-treated mice. Conclusions This study demonstrates that PJH prevents respiratory inflammation and airway remodeling caused by CS with LPS exposure suggesting potential therapy for the treatment of COPD.

scholarly journals Yiqi Gubiao pill alleviates chronic obstructive pulmonary disease in rats via upregulation of klotho expression

2021 ◽  
Vol 19 (12) ◽  
pp. 2577-2582
Author(s):  
Zheng Li ◽  
Jing Wang ◽  
Dan Xu ◽  
Jing Jing ◽  
Fengsen Li
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Lung Damage ◽  
Enzyme Linked Immunosorbent Assay ◽  
Chronic Obstructive ◽  
High Dose ◽  
Western Blot Assay ◽  
Obstructive Pulmonary Disease ◽  
Protein Expressions

Purpose: To investigate the effect of Yiqi Gubiao pill (YGP) on chronic obstructive pulmonary disease (COPD) in rats, and the  mechanism of its action.Methods: Six groups of eight-week old male SPF-grade Wistar rats (n = 60) were used (10 rats/group), viz, control, COPD, low-dose YGP, medium-dose YGP, high-dose YGP, and dexamethasone groups. Chronic obstructive pulmonary disease (COPD) was induced using a standard method. Graded doses of YGP were prepared by dissolving 100, 200 or 400 pills of Yiqi Gubiao. Lung damage and airway remodeling were determined by histological examination. Enzyme-linked immunosorbent assay (ELISA) was used to measure levels of klotho in rat serum and bronchoalveolar lavage fluid (BALF). The mRNA and protein expressions of klotho in lung tissue were assayed with qRT-PCR) and Western blot assay, respectively.Results: Serum and BALF klotho levels were significantly lower in COPD rats than in control, but the levels were markedly and dose-dependently increased by YGP (p < 0.05). Treatment of COPD rats with YGP led to significant and dose-dependent upregulation of mRNA and protein expressions of klotho (p < 0.05). Moreover, histologic score (index of lung damage) increased in COPD rats, relative to control, but it was dose-dependently decreased by YGP (p < 0.05).Conclusion: These results suggest that YGP alleviates COPD in rats via the upregulation of klotho expression. However, the potential use of YGP for COPD still needs further clinical research. Keywords: Chronic obstructive pulmonary disease, Klotho, Lungs, Protein expression, Yiqi Gubiao pill

scholarly journals Why new biology must be uncovered to advance therapeutic strategies for chronic obstructive pulmonary disease

2021 ◽  
Vol 320 (1) ◽  
pp. L1-L11
Author(s):  
Jennifer M. K. Nguyen ◽  
Douglas N. Robinson ◽  
Venkataramana K. Sidhaye
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Airway Remodeling ◽  
Disease Onset ◽  
Health Concern ◽  
Model Organisms ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Discovery Research ◽  
Causes Of Disease

Chronic obstructive pulmonary disease (COPD) is characterized by the destruction of alveolar tissue (in emphysema) and airway remodeling (leading to chronic bronchitis), which cause difficulties in breathing. It is a growing public health concern with few therapeutic options that can reverse disease progression or mortality. This is in part because current treatments mainly focus on ameliorating symptoms induced by inflammatory pathways as opposed to curing disease. Hence, emerging research focused on upstream pathways are likely to be beneficial in the development of efficient therapeutics to address the root causes of disease. Some of these pathways include mitochondrial function, cytoskeletal structure and maintenance, and airway hydration, which are all affected by toxins that contribute to COPD. Because of the complexity of COPD and unknown targets for disease onset, simpler model organisms have proved to be useful tools in identifying disease-relevant pathways and targets. This review summarizes COPD pathology, current treatments, and therapeutic discovery research, with a focus on the aforementioned pathways that can advance the therapeutic landscape of COPD.

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