scholarly journals Pulmonary inflammation induced by low-dose particulate matter exposure in mice

2019 ◽  
Vol 317 (3) ◽  
pp. L424-L430 ◽  
Author(s):  
Yik Lung Chan ◽  
Baoming Wang ◽  
Hui Chen ◽  
Kin Fai Ho ◽  
Junji Cao ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Low Dose ◽  
Residential Buildings ◽  
Pulmonary Inflammation ◽  
Antioxidant Defense System ◽  
Epidemiological Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Manganese Superoxide ◽  
Impaired Lung Function

Air pollution is a ubiquitous problem and comprises gaseous and particulate matter (PM). Epidemiological studies have clearly shown that exposure to PM is associated with impaired lung function and the development of lung diseases, such as chronic obstructive pulmonary disease and asthma. To understand the mechanisms involved, animal models are often used. However, the majority of such models represent high levels of exposure and are not representative of the exposure levels in less polluted countries, such as Australia. Therefore, in this study, we aimed to determine whether low dose PM10 exposure has any detrimental effect on the lungs. Mice were intranasally exposed to saline or traffic-related PM10 (1μg or 5μg/day) for 3 wk. Bronchoalveolar lavage (BAL) and lung tissue were analyzed. PM10 at 1 μg did not significantly affect inflammatory and mitochondrial markers. At 5 μg, PM10 exposure increased lymphocytes and macrophages in BAL fluid. Increased NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and IL-1β production occurred following PM10 exposure. PM10 (5 μg) exposure reduced mitochondrial antioxidant manganese superoxide (antioxidant defense system) and mitochondrial fusion marker (OPA-1), while it increased fission marker (Drp-1). Autophagy marker light-chain 3 microtubule-associated protein (LC3)-II and phosphorylated-AMPK were reduced, and apoptosis marker (caspase 3) was increased. No significant change of remodeling markers was observed. In conclusion, a subchronic low-level exposure to PM can have an adverse effect on lung health, which should be taken into consideration for the planning of roads and residential buildings.

scholarly journals Chronic exposure to ambient particulate matter induces gut microbial dysbiosis in a rat COPD model

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Chronic Exposure ◽  
Pulmonary Inflammation ◽  
Short Chain Fatty Acids ◽  
Chronic Obstructive ◽  
Rat Lung ◽  
Ambient Particulate Matter ◽  
Microbial Composition ◽  
Obstructive Pulmonary Disease ◽  
Microbial Dysbiosis

Abstract Background The role of the microbiota in the pathogenesis of chronic obstructive pulmonary disease (COPD) following exposure to ambient particulate matter (PM) is largely unknown. Methods Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel (BMF), or motor vehicle exhaust (MVE) for 4, 12, and 24 weeks. We performed pulmonary inflammation evaluation, morphometric measurements, and lung function analysis in rat lung at three different times points during exposure. Lung and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified. Results After a 24-week PM exposure, rats exhibited pulmonary inflammation and pathological changes characteristic of COPD. The control and PM exposure (BMF and MVE) groups showed similar microbial diversity and composition in rat lung. However, the gut microbiota after 24 weeks PM exposure was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide. Conclusion Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.

scholarly journals Chronic Exposure to Ambient Particulate Matter Induces Gut Microbial Dysbiosis in a Rat COPD Model

2020 ◽  
Author(s):  
Naijian Li ◽  
Zhaowei Yang ◽  
Baoling Liao ◽  
Tianhui Pan ◽  
Jinding Pu ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Chronic Exposure ◽  
Pulmonary Inflammation ◽  
Short Chain Fatty Acids ◽  
Chronic Obstructive ◽  
Rat Lung ◽  
Ambient Particulate Matter ◽  
Microbial Composition ◽  
Obstructive Pulmonary Disease ◽  
Microbial Dysbiosis

Abstract Background: The role of the microbiota in the pathogenesis of chronic obstructive pulmonary disease (COPD) following exposure to ambient particulate matter (PM) is largely unknown.Methods: Fifty-four male Sprague-Dawley rats were exposed to clean air, biomass fuel (BMF), or motor vehicle exhaust (MVE) for 4, 12, and 24 weeks. We performed pulmonary inflammation evaluation, morphometric measurements, and lung function analysis in rat lung at three different times points during exposure. Lung and gut microbial composition was assessed by 16S rRNA pyrosequencing. Serum lipopolysaccharide levels were measured and short-chain fatty acids in colon contents were quantified.Results: After a 24-week PM exposure, rats exhibited pulmonary inflammation and pathological changes characteristic of COPD. The control and PM exposure (BMF and MVE) groups showed similar microbial diversity and composition in rat lung. However, the gut microbiota after 24 weeks PM exposure was characterized by decreased microbial richness and diversity, distinct overall microbial composition, lower levels of short-chain fatty acids, and higher serum lipopolysaccharide.Conclusion: Chronic exposure to ambient particulate matter induces gut microbial dysbiosis and metabolite shifts in a rat model of chronic obstructive pulmonary disease.

Screening of High-risk Patients for Chronic Obstructive Pulmonary Disease in Primary Care: A Narrative Review (Preprint)

2020 ◽  
Author(s):  
Ponrathi Athilingam ◽  
Andrew Bugajski ◽  
Usha Menon
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Lung Function ◽  
Pulmonary Disease ◽  
Current Knowledge ◽  
Screening Tools ◽  
Chronic Obstructive ◽  
Early Screening ◽  
Obstructive Pulmonary Disease ◽  
Impaired Lung Function ◽  
Risk Patients

UNSTRUCTURED Chronic obstructive pulmonary disease (COPD) predominantly affects older adults, and claimed 3 million lives in 2016, making it the third leading cause of death worldwide. Over 35 million Americans aged 40 or older have lung function consistent with diagnosable COPD. COPD and cardiovascular disease (CVD) have a bidirectional relationship, in that one is a risk factor for developing the other. National and international consortiums recommend early screening of adults at risk of COPD, such as those with CVD. Recommended screening strategies include screening tools to assess symptoms, medical history, and handheld spirometry. Handheld spirometry has high diagnostic accuracy and if impaired lung function is indicated, these patients are referred for pulmonary function testing (PFT), the diagnostic gold standard for COPD. However, there is no clinical consensus for pulmonary screening in people with CVD. Current knowledge relating to the prevalence and incidence of CVD in people with COPD and the mechanisms that underlie their coexistence is key in combating the global burden of COPD.

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 Classification of COPD patients and compliance to recommended treatment in Greece according to GOLD 2017 report: the RELICO study

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Nikolaos Tzanakis ◽  
Nikolaos Koulouris ◽  
Katerina Dimakou ◽  
Konstantinos Gourgoulianis ◽  
Epameinondas Kosmas ◽  
...  
Keyword(s):  
Chronic Obstructive Lung Disease ◽  
Chronic Obstructive ◽  
Cross Sectional ◽  
Obstructive Pulmonary Disease ◽  
Medical Practitioners ◽  
Recommended Treatment ◽  
Copd Patients ◽  
Assessment Approach ◽  
Impaired Lung Function ◽  
Group B

Abstract Background Chronic obstructive pulmonary disease (COPD) is a multifactorial clinical condition, characterized by chronic progressive (or worsening) respiratory symptoms, structural pulmonary abnormalities, and impaired lung function, and is often accompanied by multiple, clinically significant comorbid disorders. In 2017, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) issued a new report on COPD prevention, diagnosis and management, aiming at personalizing the maintenance therapeutic approach of the stable disease, based on the patients’ symptoms and history of exacerbations (ABCD assessment approach). Our objective was to evaluate the implementation of GOLD suggestions in everyday clinical practice in Greece. Methods This was a cross-sectional observational study. Sixty-five different variables (demographics, vital sign measurements, COPD-related medical history parameters, comorbidities, vaccination data, COPD severity based on spirometry measurements, COPD stage based on the ABCD assessment approach, COPD treatments) were collected from 3615 nation-wide COPD patients (Greece). Results The mean age at the time of initial COPD diagnosis was 63.8 (± 10.2). Almost 60% of the subjects were classified into group B, while the remaining patients were falling into groups A (18%) and D (21%), and only a small minority of patients belonged to Group C, according to the ABCD assessment approach. The compliance of respiratory physicians to the GOLD 2017 therapeutic suggestions is problematic, especially when it comes to COPD patients belonging to Group A. Conclusion Our data provide valuable information regarding the demographic and medical profile of COPD patients in Greece, the domains which the revised ABCD assessment approach may show some clinical significance on, and the necessity for medical practitioners dealing with COPD patients to adhere closer to international recommendations for the proper management of the disease.

scholarly journals Simultaneous Assessment of Airway Instability and Respiratory Dynamics with Low-Dose 4D-CT in Chronic Obstructive Pulmonary Disease: A Technical Note

Respiration ◽  
2014 ◽  
Vol 87 (4) ◽  
pp. 294-300 ◽  
Author(s):  
Mark O. Wielpütz ◽  
Ralf Eberhardt ◽  
Michael Puderbach ◽  
Oliver Weinheimer ◽  
Hans-Ulrich Kauczor ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Low Dose ◽  
Technical Note ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
4D Ct ◽  
Respiratory Dynamics ◽  
Simultaneous Assessment

The Effects of Oral Almitrine on Pattern of Breathing and Gas Exchange in Patients with Chronic Obstructive Pulmonary Disease

1984 ◽  
Vol 66 (4) ◽  
pp. 435-442 ◽  
Author(s):  
J. R. Stradling ◽  
C. G. Nicholl ◽  
D. Cover ◽  
E. E. Davies ◽  
J. M. B. Hughes ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Gas Exchange ◽  
Pulmonary Disease ◽  
Low Dose ◽  
Statistical Significance ◽  
Chronic Obstructive ◽  
Inspiratory Flow Rate ◽  
Obstructive Pulmonary Disease ◽  
Oxygen Breathing ◽  
Arterial Po2

1. Almitrine at a low dose of 100 mg orally significantly raises Pao2 and lowers Paco2 in patients with chronic obstructive pulmonary disease, compared with placebo, when they were breathing air or 28% oxygen. 2. The estimated ideal alveolar — arterial Po2 difference was less after almitrine compared with placebo, when patients were breathing either air or 28% oxygen. 3. After almitrine overall ventilation breathing air increased by 10% but this did not reach statistical significance. During 28% oxygen breathing almitrine hardly altered overall ventilation but the inspiratory duty cycle (Ti/Ttot.) decreased and mean inspiratory flow rate (VT/Ti) increased compared with placebo. These changes were significant on a paired t-test (P<0.05). 4. Changes in both volume and pattern of breathing may explain the improved gas exchange in the lung after almitrine.

scholarly journals Kezdeti tapasztalatok a HUNCHEST – alacsony dózisú CT-tüdőrákszűrési pilotprogrammal

2018 ◽  
Vol 159 (43) ◽  
pp. 1741-1746 ◽  
Author(s):  
Anna Kerpel-Fronius ◽  
Zsuzsanna Monostori ◽  
Diana Solymosi ◽  
Zsolt Markóczy ◽  
Lívia Rojkó ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Low Dose ◽  
Screening Programme ◽  
Lung Cancer Screening ◽  
Lung Cancer Mortality ◽  
Chronic Obstructive ◽  
International Studies ◽  
Obstructive Pulmonary Disease ◽  
Low Dose Ct ◽  
First Results

Abstract: Introduction: Lung cancer is the cause of death of around 8000 Hungarians each year. Aim: International studies have proved that low-dose CT (LDCT) screening lowers the lung cancer mortality of high risk patients. The HUNCHEST pilot study launched in 2014 studies the possibilities of a lung cancer screening programme in Hungary. The study is also aimed at showing whether there is an increased number of detected lung cancer in the subgroup with chronic obstructive pulmonary disease (COPD). Method: COPD and nonCOPD subjects, smokers and non-smokers are screened with low-dose CT in the 50–79 age group. Results and conclusion: The study is still undergoing recruitement, but in the light of the first results, the principles of the screening programme at the National Korányi Institute of Pulmonology are also presented. Orv Hetil. 2018; 159(43): 1741–1746.

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