Exposure to Air Pollution Exacerbates Inflammation in Rats with Preexisting COPD

Particulate matter with an aerodynamic diameter equal or less than 2.5 micrometers (PM2.5) is associated with the development of chronic obstructive pulmonary disease (COPD). The mechanisms by which PM2.5 accelerates disease progression in COPD are poorly understood. In this study, we aimed to investigate the effect of PM2.5 on lung injury in rats with hallmark features of COPD. Cardinal features of human COPD were induced in a rat model by repeated cigarette smoke inhalation and bacterial infection for 8 weeks. Then, from week 9 to week 16, some of these rats with COPD were subjected to real-time concentrated atmospheric PM2.5. Lung function, pathology, inflammatory cytokines, oxidative stress, and mucus and collagen production were measured. As expected, the COPD rats had developed emphysema, inflammation, and deterioration in lung function. PM2.5 exposure resulted in greater lung function decline and histopathological changes, as reflected by increased Mucin (MUC) 5ac, MUC5b, Collagen I, Collagen III, and the profibrotic cytokine α-smooth muscle-actin (SMA), transforming growth factor- (TGF-) β1 in lung tissues. PM2.5 also aggravated inflammation, increasing neutrophils and eosinophils in bronchoalveolar lavage fluid (BALF) and cytokines including Interleukin- (IL-) 1β, granulocyte-macrophage colony-stimulating factor (GM-CSF), and IL-4. The likely mechanism is through oxidative stress as antioxidants levels were decreased, whereas oxidants were increased, indicating a detrimental shift in the oxidant-antioxidant balance. Altogether, these results suggest that PM2.5 exposure could promote the development of COPD by impairing lung function and exacerbating pulmonary injury, and the potential mechanisms are related to inflammatory response and oxidative stress.

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Does physical inactivity cause chronic obstructive pulmonary disease?

Clinical Science ◽

10.1042/cs20090458 ◽

2010 ◽

Vol 118 (9) ◽

pp. 565-572 ◽

Cited By ~ 25

Author(s):

Nicholas S. Hopkinson ◽

Michael I. Polkey

Keyword(s):

Oxidative Stress ◽

Physical Activity ◽

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Pulmonary Disease ◽

Chronic Obstructive ◽

Activity Levels ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease ◽

Physical Activity Levels

COPD (chronic obstructive pulmonary disease) is the most common pulmonary disease and is the only common cause of death in which mortality is presently rising. It is caused by the inhalation of smoke, which leads to oxidative stress and inflammation both in the lungs and systemically. Reduced physical activity is a well-recognized consequence of the condition, but we argue here that inactivity is itself an early cause of lung function decline and symptoms. This hypothesis is supported by data from population studies that link activity levels to decline in spirometric indices, both in smokers and non-smokers. In addition, smokers with low physical activity levels are more likely to be diagnosed subsequently with COPD. Physical exercise reduces oxidative stress, has an anti-inflammatory effect and reduces the frequency of upper respiratory tract infections, providing a number of mechanisms by which it could attenuate the harmful effects of smoking. There is sufficient evidence to justify population trials of lifestyle interventions aimed at improving physical activity levels and reducing lung function decline in people diagnosed with early COPD through spirometry screening.

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Bronchoalveolar lavage fluid concentrations of transforming growth factor (TGF)-beta1, TGF-beta2, interleukin (IL)-4 and IL-13 after segmental allergen challenge and their effects on alpha-smooth muscle actin and collagen III synthesis by primary human lung fibroblasts

Clinical & Experimental Allergy ◽

10.1111/j.1365-2222.2004.01885.x ◽

2004 ◽

Vol 34 (3) ◽

pp. 437-444 ◽

Cited By ~ 126

Author(s):

V. Batra ◽

A. I. Musani ◽

A. T. Hastie ◽

S. Khurana ◽

K. A. Carpenter ◽

...

Keyword(s):

Bronchoalveolar Lavage Fluid ◽

Transforming Growth Factor ◽

Human Lung ◽

Smooth Muscle Actin ◽

Allergen Challenge ◽

Lavage Fluid ◽

Lung Fibroblasts ◽

Alpha Smooth Muscle Actin ◽

Collagen Iii ◽

Segmental Allergen Challenge

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

BMC Pulmonary Medicine ◽

10.1186/s12890-021-01409-6 ◽

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.

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RISK FACTORS OF INCREASING LUNG FUNCTION DECLINE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A REAL-WORLD ANALYSIS

Respirology ◽

10.1111/resp.13207_425 ◽

2017 ◽

Vol 22 ◽

pp. 248-248

Keyword(s):

Risk Factors ◽

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Pulmonary Disease ◽

Real World ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease

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Effect of Liuweibuqi Capsules in Pulmonary Alveolar Epithelial Cells and COPD Through JAK/STAT Pathway

Cellular Physiology and Biochemistry ◽

10.1159/000481558 ◽

2017 ◽

Vol 43 (2) ◽

pp. 743-756 ◽

Cited By ~ 8

Author(s):

Chengyang Wang ◽

Huanzhang Ding ◽

Xiao Tang ◽

Zegeng Li ◽

Lei Gan

Keyword(s):

Lung Function ◽

Cell Viability ◽

Inflammatory Cytokines ◽

Transforming Growth Factor ◽

Interferon Γ ◽

Normal Group ◽

Alveolar Epithelial Cells ◽

Chronic Obstructive ◽

Model Control ◽

Stat Pathway

Background/Aims: To evaluate the effect of Liuweibuqi capsules on chronic obstructive pulmonary disease (COPD) through the JAK/STAT pathway. Methods: Lung function was measured with a spirometer. Changes in lung histology were observed using H&E staining. Cigarette smoke extract combined with lipopolysaccharide (CSE+LPS) was used to establish the cellular COPD model. Cytokine levels were determined using ELISA, and changes in the JAK/STAT pathway were evaluated using western blotting. The CCK8 method and flow cytometry were used to measure cell viability and apoptosis, respectively. Results: Liuweibuqi capsules reduced the damage in the lung tissues and the loss of lung function in the COPD rats. Additionally, the levels of interleukin (IL)-1β, interferon γ (IFNγ), IL-6, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β1 were higher, whereas IL-10 was lower in the model control (MC) and CSE+LPS groups than in the normal group. The phosphorylation levels of JAK1, JAK2, STAT1, STAT3 and STAT5 were higher and the levels of SOCS1 and SOCS3 were lower in the MC group and CSE+LPS group compared with the normal group. After Liuweibuqi capsule treatment, the expression of inflammatory cytokines and elements of the JAK/STAT pathway were lower. In addition, over-expression of STAT3 blocked the effects of the Liuweibuqi capsules on the release of inflammatory cytokines, cell viability and apoptosis. Conclusion: Our findings suggested that Liuweibuqi capsule might effectively ameliorate the progression of COPD via the JAK/STAT pathway.

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Lung function, forced expiratory volume in 1 s decline and COPD hospitalisations over 44 years of follow-up

European Respiratory Journal ◽

10.1183/13993003.01575-2015 ◽

2015 ◽

Vol 47 (3) ◽

pp. 742-750 ◽

Cited By ~ 8

Author(s):

Suneela Zaigham ◽

Per Wollmer ◽

Gunnar Engström

Keyword(s):

Lung Function ◽

Airflow Obstruction ◽

Fixed Ratio ◽

Population Based ◽

Forced Expiratory Volume ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease ◽

Hazard Ratios

The use of baseline lung function in the prediction of chronic obstructive pulmonary disease (COPD) hospitalisations, all-cause mortality and lung function decline was assessed in the population-based “Men Born in 1914” cohort.Spirometry was assessed at age 55 years in 689 subjects, of whom 392 had spirometry reassessed at age 68 years. The cohort was divided into three groups using fixed ratio (FR) and lower limit of normal (LLN) criterion: forced expiratory volume in 1 s (FEV1)/vital capacity (VC) ≥70%, FEV1/VC <70% but ≥LLN (FR+LLN−), and FEV1/VC <70% and <LLN (FR+LLN+).Over 44 years of follow-up, 88 men were hospitalised due to COPD and 686 died. Hazard ratios (95% CI) for incident COPD hospitalisation were 4.15 (2.24–7.69) for FR+LLN− and 7.88 (4.82–12.87) for FR+LLN+ (reference FEV1/VC ≥70%). Hazard ratios for death were 1.30 (0.98–1.72) for FR+LLN− and 1.58 (1.25–2.00) for FR+LLN+. The adjusted FEV1 decline between 55 and 68 years of age was higher for FR+LLN− and FR+LLN+ relative to the reference. Of those with FR+LLN− at 55 years, 53% had progressed to the FR+LLN+ group at 68 years.Airflow obstruction at age 55 years is a powerful risk factor for future COPD hospitalisations. The FR+LLN− group should be carefully evaluated in clinical practice in relation to future risks and potential benefit from early intervention. This is reinforced by the increased FEV1 decline in this group.

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Global Initiative for Chronic Obstructive Lung Disease 2017 Classification and Lung Function Decline in Chronic Obstructive Pulmonary Disease

American Journal of Respiratory and Critical Care Medicine ◽

10.1164/rccm.201706-1154le ◽

2018 ◽

Vol 197 (5) ◽

pp. 670-673 ◽

Cited By ~ 11

Author(s):

Wan C. Tan ◽

Jean Bourbeau ◽

Shawn D. Aaron ◽

Guohai Zhou ◽

Francois Maltais ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Lung Disease ◽

Pulmonary Disease ◽

Obstructive Lung Disease ◽

Chronic Obstructive Lung Disease ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease ◽

Global Initiative

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BMI is associated with FEV1 decline in chronic obstructive pulmonary disease: a meta-analysis of clinical trials

Respiratory Research ◽

10.1186/s12931-019-1209-5 ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 16

Author(s):

Yilan Sun ◽

Stephen Milne ◽

Jen Erh Jaw ◽

Chen Xi Yang ◽

Feng Xu ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Clinical Trials ◽

Lung Function ◽

Protective Effect ◽

Obesity Paradox ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease ◽

Meta Regression ◽

The Relationship

Abstract Background There is considerable heterogeneity in the rate of lung function decline in chronic obstructive pulmonary disease (COPD), the determinants of which are largely unknown. Observational studies in COPD indicate that low body mass index (BMI) is associated with worse outcomes, and overweight/obesity has a protective effect – the so-called “obesity paradox”. We aimed to determine the relationship between BMI and the rate of FEV1 decline in data from published clinical trials in COPD. Methods We performed a systematic review of the literature, and identified 5 randomized controlled trials reporting the association between BMI and FEV1 decline. Four of these were included in the meta-analyses. We analyzed BMI in 4 categories: BMI-I (< 18.5 or < 20 kg/m2), BMI-II (18.5 or 20 to < 25 kg/m2), BMI-III (25 to < 29 or < 30 kg/m2) and BMI-IV (≥29 or ≥ 30 kg/m2). We then performed a meta-regression of all the estimates against the BMI category. Results The estimated rate of FEV1 decline decreased with increasing BMI. Meta-regression of the estimates showed that BMI was significantly associated with the rate of FEV1 decline (linear trend p = 1.21 × 10− 5). Conclusions These novel findings support the obesity paradox in COPD: compared to normal BMI, low BMI is a risk factor for accelerated lung function decline, whilst high BMI has a protective effect. The relationship may be due to common but as-of-yet unknown causative factors; further investigation into which may reveal novel endotypes or targets for therapeutic intervention.

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Role of Diet in Chronic Obstructive Pulmonary Disease Prevention and Treatment

Nutrients ◽

10.3390/nu11061357 ◽

2019 ◽

Vol 11 (6) ◽

pp. 1357 ◽

Cited By ~ 14

Author(s):

Egeria Scoditti ◽

Marika Massaro ◽

Sergio Garbarino ◽

Domenico Maurizio Toraldo

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Pulmonary Disease ◽

Dietary Patterns ◽

Scientific Evidence ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease ◽

Prevention And Treatment ◽

The Impact

Chronic obstructive pulmonary disease is one of the leading causes of morbidity and mortality worldwide and a growing healthcare problem. Identification of modifiable risk factors for prevention and treatment of COPD is urgent, and the scientific community has begun to pay close attention to diet as an integral part of COPD management, from prevention to treatment. This review summarizes the evidence from observational and clinical studies regarding the impact of nutrients and dietary patterns on lung function and COPD development, progression, and outcomes, with highlights on potential mechanisms of action. Several dietary options can be considered in terms of COPD prevention and/or progression. Although definitive data are lacking, the available scientific evidence indicates that some foods and nutrients, especially those nutraceuticals endowed with antioxidant and anti-inflammatory properties and when consumed in combinations in the form of balanced dietary patterns, are associated with better pulmonary function, less lung function decline, and reduced risk of COPD. Knowledge of dietary influences on COPD may provide health professionals with an evidence-based lifestyle approach to better counsel patients toward improved pulmonary health.

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