scholarly journals Acebrophylline: an airway mucoregulator and anti-inflammatory agent

2016 ◽  
Vol 67 (2) ◽  
Author(s):  
E. Pozzi
Keyword(s):  
Chronic Bronchitis ◽  
Bronchial Hyperresponsiveness ◽  
Airway Disease ◽  
Blood Levels ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
Antiinflammatory Action ◽  
Surfactant Production ◽  
Β2 Agonists

Acebrophylline is an airway mucus regulator with antiinflammatory action. The drug’s approach involves several points of attack in obstructive airway disease. The molecule contains ambroxol, which facilitates various steps in the biosynthesis of pulmonary surfactant, theophylline-7 acetic acid whose carrier function raises blood levels of ambroxol, thus rapidly and intensely stimulating surfactant production. The resulting reduction in the viscosity and adhesivity of the mucus greatly improves ciliary clearance. By deviating phosphatidylcholine towards surfactant synthesis, making it no longer available for the synthesis of inflammatory mediators such as the leukotrienes, acebrophylline also exerts an inflammatory effect. This is confirmed in vivo by the reduction in aspecific bronchial hyperresponsiveness in patients with stable bronchial asthma. On a clinical level, acebrophylline is therapeutically effective in patients with acute or chronic bronchitis, chronic obstructive or asthma-like bronchitis and recurrence of chronic bronchitis; it reduces the frequency of episodes of bronchial obstruction and reduces the need for β2-agonists, and improves indexes of ventilatory function.

Possibilities of cardiovascular events in patients with chronic obstructive pulmonary disease and newly diagnosed tuberculosis, including those associated with HIV infection, when prescribing long-acting β2-agonists

MedAlliance ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 32-39
Keyword(s):  
Blood Pressure ◽  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
External Respiration ◽  
Obstructive Pulmonary Disease ◽  
Tb Treatment ◽  
Long Acting ◽  
Β2 Agonists

Chronic obstructive pulmonary disease (COPD) and pulmonary tuberculosis (TB) are a common pathology among respiratory diseases. Both conditions may have common risk factors, aggravating each other, accom-panied by the development of bronchial obstructive syndrome, requiring mandatory medical correction to increase the effectiveness of therapy for both the main and concomitant pathologies. The aim of the study was to study the effectiveness of treatment of TB in patients with COPD first diagnosed with tuberculosis, including those associated with HIV when prescribing long-acting β2-agonists. Materials and methods. A simple com-parative study included 60 patients of a TB dispensary aged 30–65 years. Patients were divided into 2 groups of 30 people (TB+COPD and TB+COPD+HIV), each of whom for 2 months received a long-acting β-agonist (indacaterol) as an accompanying therapy for the cor-rection of bronchial obstructive syndrome (BOS), with subsequent assessment of the effectiveness of therapy. Results. Subjectively, patients of both groups noted the rapid development of positive dynamics (short-ness of breath decreased from 1–3 days of taking the drug, coughing — within a week, tolerance to physical exertion improved), which was confirmed by indica-tors of the function of external respiration (FEV1). The state of the cardiovascular system was assessed by the results of daily monitoring of blood pressure (BPM). In the COPD+TB group, there is a certain average daily systolic blood pressure (SBP) with a tendency to nor-malize indicators, which is possibly associated with a decrease in the severity of hypoxia during bronchodi-lator therapy. In the COPD+TB+HIV group, the average daily level of SBP increased by 1 mm Hg, but given the very low starting rates, the increase in blood pressure had a positive effect on the patients' condition. The average heart rate (HR) during bronchodilator thera-py did not tend to increase. The best TB treatment re-sults were obtained in the TB+COPD group. In terms of the closure rate of TB+COPD decay cavities — 26.6%, TB+COPD+HIV — 20.0%), the TB+COPD+HIV group had longer periods of abacillation and closure of decay cav-ities, which is associa ted with the severity of the under-lying and associated diseases. The drug was well toler-ated in both groups. Conclusion. The use of 300 mcg long-acting β-adrenomimetics in the complex therapy of β2-adrenergic agonists for patients with TB+COPD and TB+ COPD+HIV can reduce the severity of bronchial obstruction syndrome, improve quality of life, increase adherence to TB treatment, thereby shortening hospi-talization and reduce the likelihood of disability of pa-tients, without the development of side effects from other organs and systems.

scholarly journals The neutrophil-mobilizing cytokine interleukin-26 in the airways of long-term tobacco smokers

2018 ◽  
Vol 132 (9) ◽  
pp. 959-983 ◽  
Author(s):  
Karlhans Fru Che ◽  
Ellen Tufvesson ◽  
Sara Tengvall ◽  
Elisa Lappi-Blanco ◽  
Riitta Kaarteenaho ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Bronchitis ◽  
Pathogenic Bacteria ◽  
Cell Model ◽  
Water Soluble ◽  
Chronic Obstructive ◽  
Neutrophil Accumulation

Long-term tobacco smokers with chronic obstructive pulmonary disease (COPD) or chronic bronchitis display an excessive accumulation of neutrophils in the airways; an inflammation that responds poorly to established therapy. Thus, there is a need to identify new molecular targets for the development of effective therapy. Here, we hypothesized that the neutrophil-mobilizing cytokine interleukin (IL)-26 (IL-26) is involved in airway inflammation amongst long-term tobacco smokers with or without COPD, chronic bronchitis or colonization by pathogenic bacteria. By analyzing bronchoalveolar lavage (BAL), bronchail wash (BW) and induced sputum (IS) samples, we found increased extracellular IL-26 protein in the airways of long-term smokers in vivo without further increase amongst those with clinically stable COPD. In human alveolar macrophages (AM) in vitro, the exposure to water-soluble tobacco smoke components (WTC) enhanced IL-26 gene and protein. In this cell model, the same exposure increased gene expression of the IL-26 receptor complex (IL10R2 and IL20R1) and nuclear factor κ B (NF-κB); a proven regulator of IL-26 production. In the same cell model, recombinant human IL-26 in vitro caused a concentration-dependent increase in the gene expression of NF-κB and several pro-inflammatory cytokines. In the long-term smokers, we also observed that extracellular IL-26 protein in BAL samples correlates with measures of lung function, tobacco load, and several markers of neutrophil accumulation. Extracellular IL-26 was further increased in long-term smokers with exacerbations of COPD (IS samples), with chronic bronchitis (BAL samples ) or with colonization by pathogenic bacteria (IS and BW samples). Thus, IL-26 in the airways emerges as a promising target for improving the understanding of the pathogenic mechanisms behind several pulmonary morbidities in long-term tobacco smokers.

scholarly journals A relationship between chronic obstructive pulmonary disease, obesity and melatonin level

2018 ◽  
Vol 28 (3) ◽  
pp. 359-367 ◽  
Author(s):  
A. V. Budnevskiy ◽  
Е. S. Ovsyannikov ◽  
Ya. S. Shkatova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Systemic Inflammation ◽  
Clinical Course ◽  
Antioxidant Activities ◽  
Blood Levels ◽  
Chronic Obstructive ◽  
Melatonin Level ◽  
Bronchial Obstruction ◽  
Obstructive Pulmonary Disease

This is a review of experimental and clinical studies investigated effects of obesity on clinical course of chronic obstructive pulmonary disease (COPD); pathophysiological mechanisms of this effect, and relationships between melatonin level and the course of COPD have been also discussed. Associations between severity of COPD, rate of exacerbations and blood levels of most important adipokines, such as leptin and adiponectin, and relationships between melatonin levels and those adipokines were published. Conflicting results were obtained in studies of effects of obesity on clinical course of COPD. The "obesity paradox", that is a reduction in mortality and milder bronchial obstruction in obese COPD patients, has been identified in several studies. Despite contradictory results, obesity is likely to improve prognosis of COPD due to decrease in the systemic inflammation. Levels of leptin and adiponectin increase in acute exacerbation of COPD and then decrease to the baseline. Moreover, melatonin is suggested to play a great role for COPD course, mostly due to antiinflammatory and antioxidant activities. According to results of several studies, melatonin could affect blood levels of adiponectin and lectin; this could indirectly influence on the systemic inflammation in COPD. Further studies are needed to elicit these relationships. 

scholarly journals Airway remodeling in ferrets with cigarette smoke-induced COPD using µCT imaging

2020 ◽  
Vol 319 (1) ◽  
pp. L11-L20 ◽  
Author(s):  
Denise Stanford ◽  
Harrison Kim ◽  
Sandeep Bodduluri ◽  
Jennifer LaFontaine ◽  
Stephen A. Byzek ◽  
...  
Keyword(s):  
Chronic Bronchitis ◽  
Cigarette Smoke ◽  
Structural Changes ◽  
Morphological Changes ◽  
Airway Remodeling ◽  
Chronic Obstructive ◽  
Luminal Diameter ◽  
Bronchial Wall ◽  
Wall Area

Structural changes to airway morphology, such as increased bronchial wall thickness (BWT) and airway wall area, are cardinal features of chronic obstructive pulmonary disease (COPD). Ferrets are a recently established animal model uniquely exhibiting similar clinical and pathological characteristics of COPD as humans, including chronic bronchitis. Our objective was to develop a microcomputed tomography (µCT) method for evaluating structural changes to the airways in ferrets and assess whether the effects of smoking induce changes consistent with chronic bronchitis in humans. Ferrets were exposed to mainstream cigarette smoke or air control twice daily for 6 mo. µCT was conducted in vivo at 6 mo; a longitudinal cohort was imaged monthly. Manual measurements of BWT, luminal diameter (LD), and BWT-to-LD ratio (BWT/LD) were conducted and confirmed by a semiautomated algorithm. The square root of bronchial wall area (√WA) versus luminal perimeter was determined on an individual ferret basis. Smoke-exposed ferrets reproducibly demonstrated 34% increased BWT ( P < 0.001) along with increased LD and BWT/LD versus air controls. Regression indicated that the effect of smoking on BWT persisted despite controlling for covariates. Semiautomated measurements replicated findings. √WA for the theoretical median airway luminal perimeter of 4 mm (Pi4) was elevated 4.4% in smoke-exposed ferrets ( P = 0.015). Increased BWT and Pi4 developed steadily over time. µCT-based airway measurements in ferrets are feasible and reproducible. Smoke-exposed ferrets develop increased BWT and Pi4, changes similar to humans with chronic bronchitis. µCT can be used as a significant translational platform to measure dynamic airway morphological changes.

Characteristics of Bronchial Obstruction in Patients with Chronic Obstructive Pulmonary Disease, Depending on the Comorbidity with CHD

2016 ◽  
pp. 94-97
Author(s):  
Olena Kolesnikova
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Bronchial Hyperresponsiveness ◽  
Stage Ii ◽  
Chronic Obstructive ◽  
Bronchial Obstruction ◽  
Obstructive Pulmonary Disease ◽  
Exertional Angina ◽  
Group 2 ◽  
Artery Disease

The objective: to study the basic spirometry and pneumotachometry in patients with isolated COPD and patients with COPD combined with coronary artery disease. Patients and methods. A total of 3 groups of patients: group 1 – 43 patients with stage II COPD and concomitant coronary heart disease, stable exertional angina (SEA) FC II, group 2 – 47 patients with stage II COPD and group 3 – 26 patients with coronary artery disease, CCH FC II. Results. It is found that in COPD presence of coronary artery disease associated with a statistically significant lower rates VC, PIF, MIF at 25%, 50%, 75% FVC as well as a statistically significant reduction MEF in the interval from 25% to 75% FVC compared with those of patients with isolated over COPD. Conclusion. The presence of coronary artery disease, stable angina FC II patients with COPD II stage. It is associated with more severe bronchial hyperresponsiveness and more pronounced decrease in VC, FVC, FEV1, ratios of FEV1/FVC, and significantly more pronounced changes in bronchial obstruction in the form of reduced rates of PIF, MIF25, MIF50, MIF75, MEF25175 compared with their values in patients with COPD isolated passage.

scholarly journals In vivo endomicroscopic features of distal airways in chronic bronchitis and chronic obstructive pulmonary disease

2018 ◽  
Vol 9 (4) ◽  
pp. 15-24
Author(s):  
O. V. Danilevskaya ◽  
A. V. Averyanov
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Chronic Bronchitis ◽  
Pulmonary Disease ◽  
Lung Diseases ◽  
Diagnostic Methods ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

Relevance: Probe-based confocal laser endomicroscopy (CLE) of distal airways is a unique technology that allows real-time visualization of structures containing natural fluorophores, which are emitted by exposure to laser radiation with a wavelength of 488 nm, in vivo. To date, the endomicroscopic features of the distal respiratory tract have not been adequately studied in lung diseases, including chronic obstructive pulmonary disease and chronic bronchitis. The goal of the present study is to describe the endomicroscopic signs of the distal parts of the respiratory system in chronic inflammatory lung diseases such as chronic obstructive pulmonary disease and chronic bronchitis. Methods: A total of 21 patients with emphysematous and bronchitic phenotypes of chronic obstructive pulmonary disease and chronic bronchitis were examined. All the patients have undergone CLE of distal airways or alveoloscopy during bronchoscopy. The most pathognomonic changes were evaluated on the obtained endomicroscopic images. Results: For each studied nosological form of chronic inflammatory lung diseases, by careful morphometric analysis of a significant number of informative images, the most specific endomicroscopic changes were identified with the release of CLE patterns. Conclusions: CLE of distal airways in patients with chronic inflammatory lung diseases allows visualizing changes in the elastic framework of the acini, as well as identifying pathological intraluminal contents, which can be attributed to valuable additional tools in a row of diagnostic methods of respiratory medicine.

scholarly journals Air Pollution and the Airways: Lessons from a Century of Human Urbanization

Atmosphere ◽  
2021 ◽  
Vol 12 (7) ◽  
pp. 898
Author(s):  
Janne Goossens ◽  
Anne-Charlotte Jonckheere ◽  
Lieven J. Dupont ◽  
Dominique M. A. Bullens
Keyword(s):  
Air Pollution ◽  
Industrial Revolution ◽  
Defense Mechanism ◽  
Airway Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Airway Symptoms ◽  
Neurological System

Since the industrial revolution, air pollution has become a major problem causing several health problems involving the airways as well as the cardiovascular, reproductive, or neurological system. According to the WHO, about 3.6 million deaths every year are related to inhalation of polluted air, specifically due to pulmonary diseases. Polluted air first encounters the airways, which are a major human defense mechanism to reduce the risk of this aggressor. Air pollution consists of a mixture of potentially harmful compounds such as particulate matter, ozone, carbon monoxide, volatile organic compounds, and heavy metals, each having its own effects on the human body. In the last decades, a lot of research investigating the underlying risks and effects of air pollution and/or its specific compounds on the airways, has been performed, involving both in vivo and in vitro experiments. The goal of this review is to give an overview of the recent data on the effects of air pollution on healthy and diseased airways or models of airway disease, such as asthma or chronic obstructive pulmonary disease. Therefore, we focused on studies involving pollution and airway symptoms and/or damage both in mice and humans.

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.

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