Ephedrine ameliorates chronic obstructive pulmonary disease (COPD) through restraining endoplasmic reticulum (ER) stress in vitro and in vivo

2022 ◽  
Vol 103 ◽  
pp. 107842
Author(s):  
Hong-Lei Wang ◽  
Fen-Qiao Chen ◽  
Li-Juan Wu
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals The Involvement of Phospholipases A2in Asthma and Chronic Obstructive Pulmonary Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Ewa Pniewska ◽  
Rafal Pawliczak
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Animal Models ◽  
Pulmonary Disease ◽  
Cell Cultures ◽  
Inflammatory Diseases ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Chronic Inflammatory Diseases

The increased morbidity, mortality, and ineffective treatment associated with the pathogenesis of chronic inflammatory diseases such as asthma and chronic obstructive pulmonary disease (COPD) have generated much research interest. The key role is played by phospholipases from the A2superfamily: enzymes which are involved in inflammation through participation in pro- and anti-inflammatory mediators production and have an impact on many immunocompetent cells. The 30 members of the A2superfamily are divided into 7 groups. Their role in asthma and COPD has been studiedin vitroandin vivo(animal models, cell cultures, and patients). This paper contains complete and updated information about the involvement of particular enzymes in the etiology and course of asthma and COPD.

scholarly journals miR-4456/CCL3/CCR5 Pathway in the Pathogenesis of Tight Junction Impairment in Chronic Obstructive Pulmonary Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Weiwei Yu ◽  
Ting Ye ◽  
Jie Ding ◽  
Yi Huang ◽  
Yang Peng ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Tight Junction ◽  
Pulmonary Disease ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Healthy Controls ◽  
Rt Pcr ◽  
Obstructive Pulmonary Disease

Background: Cigarette smoke exposure (CSE) is a major cause of chronic obstructive pulmonary disease (COPD). The smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the tight junction (TJ) proteins. Even though the inflammatory mechanism of chemokine (C-C motif) ligand 3 (CCL3) in COPD has gained increasing attention in the research community, however, the underlying signaling pathway, remains unknown.Objectives: To identify the relationship of CCL3 in the pathogenesis of tight junction impairment in COPD and the pathway through which CSE causes damage to TJ in COPD via CCL3, both in vivo and in vitro.Methods: We screened the inflammatory factors in the peripheral blood mononuclear cells (PBMCs) from healthy controls and patients at each GOLD 1-4 stage of chronic obstructive pulmonary disease. RT-PCR, western blot, and ELISA were used to detect the levels of CCL3, ZO-1, and occludin after Cigarette smoke exposure. Immunofluorescence was applied to examine the impairment of the TJs in 16-HBE and A549 cells. The reverse assay was used to detect the effect of a CCR5 antagonist (DAPTA) in COPD. In the CSE-induced COPD mouse model, H&E staining and lung function tests were used to evaluate the pathological and physical states in each group. Immunofluorescence was used to assess the impairment of TJs in each group. ELISA and RT-PCR were used to examine the mRNA or protein expression of CCL3 or miR-4456 in each group.Results: The in vivo and in vitro results showed that CCL3 expression was increased in COPD compared with healthy controls. CCL3 caused significant injury to TJs through its C-C chemokine receptor type 5 (CCR5), while miR-4456 could suppress the effect of CCL3 on TJs by binding to the 3′-UTR of CCL3.Conclusion: miR-4456/CCL3/CCR5 pathway may be a potential target pathway for the treatment of COPD.

In vivo neutrophil sequestration within lungs of humans is determined by in vitro "filterability"

1991 ◽  
Vol 71 (5) ◽  
pp. 1996-2003 ◽  
Author(s):  
C. Selby ◽  
E. Drost ◽  
P. K. Wraith ◽  
W. MacNee
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Normal Subjects ◽  
Chronic Obstructive ◽  
Cell Deformability ◽  
Obstructive Pulmonary Disease ◽  
Neutrophil Sequestration ◽  
In Transit

Neutrophils are normally delayed in transit through the lung microcirculation, relative to the passage of erythrocytes. This sequestration contributes to a pulmonary pool of neutrophils that may relate to the relative inability of neutrophils to deform compared with erythrocytes when in transit in the pulmonary capillaries. A micropore membrane was used to model the human pulmonary microcirculation, in which cell deformability was measured as the pressure developed during filtration of the cells through the membrane at a constant flow. We demonstrated a significant correlation between in vitro deformability and in vivo lung sequestration of indium-111-labeled neutrophils in 10 normal subjects (r = 0.69, P less than 0.02). In eight patients with stable chronic obstructive pulmonary disease, this relationship was not significant (r = -0.2, P greater than 0.05). Furthermore, in a subject with microscopic pulmonary telangiectasia known to allow significant passage of 30-microns microspheres, neutrophils passed through the lungs without delay. Moreover, neutrophils from patients studied acutely with an exacerbation of chronic obstructive pulmonary disease were temporarily less deformable (P less than 0.01). These studies confirm that cell deformability is an important determinant of the normal neutrophil sequestration within the lungs. Changes in cell deformability may alter the extent of this sequestration.

scholarly journals Tocotrienols: Dietary Supplements for Chronic Obstructive Pulmonary Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 883
Author(s):  
Xiangming Ji ◽  
Hongwei Yao ◽  
Maureen Meister ◽  
Douglas S. Gardenhire ◽  
Huanbiao Mo
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Chronic Bronchitis ◽  
Pulmonary Disease ◽  
Significant Risk ◽  
Chronic Obstructive ◽  
Alveolar Wall ◽  
Obstructive Pulmonary Disease ◽  
Anti Inflammatory

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide. Emphysema and chronic bronchitis are the two major phenotypes of COPD, which have many symptoms, such as dyspnea, chronic cough, and mucus overproduction. Emphysema is characterized by the destruction of the alveolar wall, while chronic bronchitis is characterized by limitations in expiratory airflow. Cigarette smoking is the most significant risk factor for the pathogenesis of COPD in the developed world. Chronic inflammation contributes to the onset and progression of the disease and furthers the risk of comorbidities. Current treatment options and prevention strategies for COPD are very limited. Tocotrienols are a group of vitamin E molecules with antioxidant and anti-inflammatory properties. Individual tocotrienols (α, γ, and δ) have shown their ability to attenuate inflammation specifically via suppressing nuclear factor-κB-mediated cytokine production. The δ- and γ-forms of tocotrienols have been indicated as the most effective in the prevention of macrophage infiltration, production of reactive oxygen species, and cytokine secretion. This review briefly discusses the pathogenesis of COPD and the role of inflammation therein. Furthermore, we summarize the in vitro and in vivo evidence for the anti-inflammatory activity of tocotrienols and their potential application to COPD management. Coupled with the bioavailability and safety profile of tocotrienols, the ability of these compounds to modulate COPD progression by targeting the inflammation pathways renders them potential candidates for novel therapeutic approaches in the treatment of COPD patients.

scholarly journals Role of bronchodilation and pattern of breathing in increasing tidal expiratory flow with progressive induced hypercapnia in chronic obstructive pulmonary disease

2018 ◽  
Vol 124 (1) ◽  
pp. 91-98
Author(s):  
Kevin E. Finucane ◽  
Bhajan Singh
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Esophageal Pressure ◽  
Forced Expiratory Volume ◽  
Chronic Obstructive ◽  
Elastic Recoil ◽  
Obstructive Pulmonary Disease ◽  
Recoil Pressure

Hypercapnia (HC) in vitro relaxes airway smooth muscle; in vivo, it increases respiratory effort, tidal expiratory flows (V̇exp), and, by decreasing inspiratory duration (Ti), increases elastic recoil pressure (Pel) via lung viscoelasticity; however, its effect on airway resistance is uncertain. We examined the contributions of bronchodilation, Ti, and expiratory effort to increasing V̇exp with progressive HC in 10 subjects with chronic obstructive pulmonary disease (COPD): mean forced expiratory volume in 1 s (FEV1) 53% predicted. Lung volumes (Vl), V̇exp, esophageal pressure (Pes), Ti, and end-tidal Pco2 ([Formula: see text]) were measured during six tidal breaths followed by an inspiratory capacity (IC), breathing air, and at three levels of HC. V̇exp and V̇ with submaximal forced vital capacities breathing air (V̇sFVC) were compared. Pulmonary resistance ( Rl) was measured from the Pes-V̇ relationship. V̇exp and Pes at end-expiratory lung volume (EELV) + 0.3 tidal volume [V̇(0.3Vt) and Pes(0.3Vt), respectively], Ti, and Rl correlated with [Formula: see text] ( P < 0.001 for all) and were independent of tiotropium. [Formula: see text], Ti, and Pes(0.3Vt) predicted the increasing V̇(0.3Vt)/V̇sFVC(0.3Vt) [multiple regression analysis (MRA): P = 0.001, 0.004, and 0.025, respectively]. At [Formula: see text] ≥ 50 Torr, V̇(0.3Vt)/V̇sFVC(0.3Vt) exceeded unity in 30 of 36 measurements and was predicted by [Formula: see text] and Pes(0.3Vt) (MRA: P = 0.02 and 0.025, respectively). Rl decreased at [Formula: see text] 45 Torr ( P < 0.05) and did not change with further HC. IC and Vl(0.3Vt) did not change with HC. We conclude that in COPD HC increases V̇exp due to bronchodilation, increased Pel secondary to decreasing Ti, and increased expiratory effort, all promoting lung emptying and a stable EELV. NEW & NOTEWORTHY The response of airways to intrapulmonary hypercapnia (HC) is uncertain. In chronic obstructive pulmonary disease (COPD), progressive HC increases tidal expiratory flows by inducing bronchodilation and via an increased rate of inspiration and lung viscoelasticity, a probable increase in lung elastic recoil pressure, both changes increasing expiratory flows, promoting lung emptying and a stable end-expiratory volume. Bronchodilation with HC occurred despite optimal standard bronchodilator therapy, suggesting that in COPD further bronchodilation is possible.

scholarly journals Proteases and Their Inhibitors in Chronic Obstructive Pulmonary Disease

2018 ◽  
Vol 7 (9) ◽  
pp. 244 ◽  
Author(s):  
Tapan Dey ◽  
Jatin Kalita ◽  
Sinéad Weldon ◽  
Clifford Taggart
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Drug Development ◽  
Pulmonary Disease ◽  
Current Status ◽  
Chronic Obstructive ◽  
Future Prospects ◽  
Obstructive Pulmonary Disease ◽  
Drug Molecules

In the context of respiratory disease, chronic obstructive pulmonary disease (COPD) is the leading cause of mortality worldwide. Despite much development in the area of drug development, currently there are no effective medicines available for the treatment of this disease. An imbalance in the protease: Antiprotease ratio in the COPD lung remains an important aspect of COPD pathophysiology and several studies have shown the efficacy of antiprotease therapy in both in vitro and in vivo COPD models. However more in-depth studies will be required to validate the efficacy of lead drug molecules targeting these proteases. This review discusses the current status of protease-directed drugs used for treating COPD and explores the future prospects of utilizing the potential of antiprotease-based therapeutics as a treatment for this disease.

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