scholarly journals Losartan does not inhibit cigarette smoke-induced lung inflammation in mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
M. L. Hepworth ◽  
S. L. Passey ◽  
H. J. Seow ◽  
R. Vlahos
Keyword(s):  
Angiotensin Ii ◽  
Mrna Expression ◽  
Lung Inflammation ◽  
Lavage Fluid ◽  
Receptor Expression ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Angiotensin Ii Receptor ◽  
Obstructive Pulmonary Disease ◽  
Cardiovascular Comorbidity

Abstract Chronic Obstructive Pulmonary Disease (COPD) is a progressive lung disease largely caused by cigarette smoking (CS) and is characterized by lung inflammation and airflow limitation that is not fully reversible. Approximately 50% of people with COPD die of a cardiovascular comorbidity and current pharmacological strategies provide little benefit. Therefore, drugs that target the lung and the cardiovascular system concurrently may be an advantageous therapeutic strategy. The aim of this study was to see whether losartan, an angiotensin-II AT1a receptor antagonist widely used to treat hypertension associated with cardiovascular disease, protects against CS-induced lung inflammation in mice. Male BALB/c mice were exposed to CS for 8 weeks and treated with either losartan (30 mg/kg) or vehicle daily. Mice were euthanized and bronchoalveolar lavage fluid (BALF) inflammation, and whole lung cytokine, chemokine and protease mRNA expression assessed. CS caused significant increases in BALF total cells, macrophages, neutrophils and whole lung IL-6, TNF-α, CXCL-1, IL-17A and MMP12 mRNA expression compared to sham-exposed mice. However, losartan only reduced CS-induced increases in IL-6 mRNA expression. Angiotensin-II receptor expression was reduced in lung tissue from CS-exposed mice. In conclusion, losartan did not inhibit CS-induced BALF cellularity despite reducing whole lung IL-6 mRNA and Ang-II receptor expression.

scholarly journals Matrine reduces cigarette smoke-induced airway neutrophilic inflammation by enhancing neutrophil apoptosis

2019 ◽  
Vol 133 (4) ◽  
pp. 551-564 ◽  
Author(s):  
Xuhua Yu ◽  
Huei Jiunn Seow ◽  
Hao Wang ◽  
Desiree Anthony ◽  
Steven Bozinovski ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Inflammation ◽  
Therapeutic Potential ◽  
Proteolytic Enzymes ◽  
Ex Vivo ◽  
Lavage Fluid ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Neutrophilic Inflammation ◽  
Anti Inflammatory

AbstractChronic Obstructive Pulmonary Disease (COPD) is a major incurable global health burden and will become the third largest cause of death in the world by 2030. It is well established that an exaggerated inflammatory and oxidative stress response to cigarette smoke (CS) leads to, emphysema, small airway fibrosis, mucus hypersecretion, and progressive airflow limitation. Current treatments have limited efficacy in inhibiting chronic inflammation and consequently do not reverse the pathology that initiates and drives the long-term progression of disease. In particular, there are no effective therapeutics that target neutrophilic inflammation in COPD, which is known to cause tissue damage by degranulation of a suite of proteolytic enzymes including neutrophil elastase (NE). Matrine, an alkaloid compound extracted from Sophora flavescens Ait, has well known anti-inflammatory activity. Therefore, the aim of the present study was to investigate whether matrine could inhibit CS-induced lung inflammation in mice. Matrine significantly reduced CS-induced bronchoalveolar lavage fluid (BALF) neutrophilia and NE activity in mice. The reduction in BALF neutrophils in CS-exposed mice by matrine was not due to reductions in pro-neutrophil cytokines/chemokines, but rather matrine’s ability to cause apoptosis of neutrophils, which we demonstrated ex vivo. Thus, our data suggest that matrine has anti-inflammatory actions that could be of therapeutic potential in treating CS-induced lung inflammation observed in COPD.

scholarly journals Herbal Formula, PM014, Attenuates Lung Inflammation in a Murine Model of Chronic Obstructive Pulmonary Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Hyojung Lee ◽  
Youngeun Kim ◽  
Hye Jin Kim ◽  
Soojin Park ◽  
Young Pyo Jang ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Murine Model ◽  
Lung Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Herbal Formula ◽  
Obstructive Pulmonary Disease ◽  
Beneficial Effects

Chronic obstructive pulmonary disease (COPD), which is characterized by airway obstruction, leads to, as the two major forms of COPD, chronic bronchitis and emphysema. This study was conducted to evaluate the effects of herbal formula, PM014, in a murine model of COPD. Balb/c mice were treated once with each herb extract in PM014 or PM014 mixture via an oral injection. Lipopolysaccharide (LPS) or elastase/LPS were administrated to the mice to induce a disease that resembles COPD. PM014 treatment significantly attenuated the increased accumulation of immune cells in bronchoalveolar lavage fluid (BALF) compared to control mice. In addition, the TNF-αand IL-6 levels in BALF were decreased in the PM014 mice. Furthermore, histological analysis demonstrated that PM014 attenuated the hazardous effects of lung inflammation. These data suggest that PM014 exerts beneficial effects against forms of COPD such as lung inflammation.

Regulatory Effects of Andrographolide on Lung Tissue Inflammation and Th17/Treg in Rats with Chronic Obstructive Pulmonary Disease Induced by Smoking and Lipopolysaccharide

2021 ◽  
Vol 11 (3) ◽  
pp. 513-519
Author(s):  
Hong Li ◽  
Shuang Song ◽  
Zhibin Kong ◽  
Zhen Zhu ◽  
Yi Liu ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Blood Cells ◽  
Lung Inflammation ◽  
White Blood Cells ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Protein Levels ◽  
Tnf Α ◽  
Monocytes And Macrophages

The pathogenesis of Chronic obstructive pulmonary disease (COPD) is complex, and lung tissue inflammation and Th17/Treg imbalance are the key factors causing lung dysfunction. We constructed a rat COPD model induced by smoking and lipopolysaccharide to explore andrographolide’s regulation on lung inflammation and Th17/Treg in COPD rats. By contrast, the study found that normal rats, COPD rats forced expiratory volume of 0.3 seconds (FEV0.3), FEV0.3/forced vital capacity (FVC), and peak expiratory flow (PEF) levels decreased. In addition, the levels of IL-8, TNF-α, IL-17, and IL-6 in alveolar lavage fluid increased, and the level of IL-10 decreased. Concurrently, the total number of white blood cells, monocytes and macrophages, neutrophils, and lymphocytes increased. Meanwhile, the contents of CD25, CD4, and Foxp3 in lung tissue all increased, and the protein levels of HMGB1, TLR4, and p65 increased. After treatment with andrographolide, the levels of FEV0.3, FEV0.3/FVC, and PEF increased, proving the increase was positively correlated with the concentration of andrographolide. The levels of IL-8, TNF-α, IL-17, and IL-6 in rat alveolar lavage fluid decreased, and the level of IL-10 sequentially. The total number of white blood cells, the number of monocytes and macrophages, the number of lymphocytes, and the neutral Granulocytes decreased significantly. And the contents of CD25, CD4, and Foxp3 in lung tissue significantly decreased, and the protein levels of HMGB1, TLR4, and p65 significantly decreased. The above results indicate that andrographolide might be a potential COPD treatment approach. Andrographolide improves the lung function of rats with COPD, reduces lung inflammation, regulates Th17/Treg balance, and its mechanism may be related to HMGB1/TLR4/NF-кB signaling.

scholarly journals Application of Proteomics and Peptidomics to COPD

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Girolamo Pelaia ◽  
Rosa Terracciano ◽  
Alessandro Vatrella ◽  
Luca Gallelli ◽  
Maria Teresa Busceti ◽  
...  
Keyword(s):  
Exhaled Breath Condensate ◽  
Lung Parenchyma ◽  
Lavage Fluid ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Exhaled Breath ◽  
Obstructive Pulmonary Disease ◽  
Disease Biomarkers ◽  
Complex Disorder ◽  
Breath Condensate

Chronic obstructive pulmonary disease (COPD) is a complex disorder involving both airways and lung parenchyma, usually associated with progressive and poorly reversible airflow limitation. In order to better characterize the phenotypic heterogeneity and the prognosis of patients with COPD, there is currently an urgent need for discovery and validation of reliable disease biomarkers. Within this context, proteomic and peptidomic techniques are emerging as very valuable tools that can be applied to both systemic and pulmonary samples, including peripheral blood, induced sputum, exhaled breath condensate, bronchoalveolar lavage fluid, and lung tissues. Identification of COPD biomarkers by means of proteomic and peptidomic approaches can thus also lead to discovery of new molecular targets potentially useful to improve and personalize the therapeutic management of this widespread respiratory disease.

scholarly journals Peranan Statin Dalam Memperbaiki Fungsi Paru pada Penyakit Paru Obstruktif Kronik (PPOK)

2017 ◽  
Vol 10 (2) ◽  
pp. 71
Author(s):  
Dina Fauzia
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Inflammation ◽  
Therapeutic Agent ◽  
Airflow Limitation ◽  
Chronic Obstructive ◽  
Systemic Diseases ◽  
Obstructive Pulmonary Disease ◽  
Parenchymal Lung Disease ◽  
Global Health Problem ◽  
Parenchymal Lung

Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fullyreversible and a global health problem with an increasing incidence. Latest pathogenesis states that inflammationoccurs in COPD is not just limited to the airway and parenchymal lung disease, but a systemic inflammation involvingother systems, especially the cardiovascular system. Therefore, the approach to COPD therapy currently includes twoaspects, suppression of lung inflammation and systemic diseases. One of the the therapeutic agent that may affectboth aspects are statin.

scholarly journals FSTL1 aggravates cigarette smoke-induced airway inflammation and airway remodeling by regulating autophagy

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ying Liu ◽  
Jiawei Xu ◽  
Tian Liu ◽  
Jinxiang Wu ◽  
Jiping Zhao ◽  
...  
Keyword(s):  
Lung Function ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Airway Remodeling ◽  
Critical Factor ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Impaired Lung Function

Abstract Background Cigarette smoke (CS) is a major risk factor for Chronic Obstructive Pulmonary Disease (COPD). Follistatin-like protein 1 (FSTL1), a critical factor during embryogenesis particularly in respiratory lung development, is a novel mediator related to inflammation and tissue remodeling. We tried to investigate the role of FSTL1 in CS-induced autophagy dysregulation, airway inflammation and remodeling. Methods Serum and lung specimens were obtained from COPD patients and controls. Adult female wild-type (WT) mice, FSTL1± mice and FSTL1flox/+ mice were exposed to room air or chronic CS. Additionally, 3-methyladenine (3-MA), an inhibitor of autophagy, was applied in CS-exposed WT mice. The lung tissues and serum from patients and murine models were tested for FSTL1 and autophagy-associated protein expression by ELISA, western blotting and immunohistochemical. Autophagosome were observed using electron microscope technology. LTB4, IL-8 and TNF-α in bronchoalveolar lavage fluid of mice were examined using ELISA. Airway remodeling and lung function were also assessed. Results Both FSTL1 and autophagy biomarkers increased in COPD patients and CS-exposed WT mice. Autophagy activation was upregulated in CS-exposed mice accompanied by airway remodeling and airway inflammation. FSTL1± mice showed a lower level of CS-induced autophagy compared with the control mice. FSTL1± mice can also resist CS-induced inflammatory response, airway remodeling and impaired lung function. CS-exposed WT mice with 3-MA pretreatment have a similar manifestation with CS-exposed FSTL1± mice. Conclusions FSTL1 promotes CS-induced COPD by modulating autophagy, therefore targeting FSTL1 and autophagy may shed light on treating cigarette smoke-induced COPD.

scholarly journals COPD Guidelines in the Asia-Pacific Regions: Similarities and Differences

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1153
Author(s):  
Shih-Lung Cheng ◽  
Ching-Hsiung Lin
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Global Strategy ◽  
Airflow Limitation ◽  
Asia Pacific ◽  
Pharmacologic Therapy ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Country Level ◽  
Similarities And Differences

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease that is associated with significant morbidity and mortality, giving rise to an enormous social and economic burden. The Global Strategy for the Diagnosis, Management and Prevention of Chronic Obstructive Pulmonary Disease (GOLD) report is one of the most frequently used documents for managing COPD patients worldwide. A survey was conducted across country-level members of Asia-Pacific Society of Respiratory (APSR) for collecting an updated version of local COPD guidelines, which were implemented in each country. This is the first report to summarize the similarities and differences among the COPD guidelines across the Asia-Pacific region. The degree of airflow limitation, assessment of COPD severity, management, and pharmacologic therapy of stable COPD will be reviewed in this report.

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