简介：AbstractChronic obstructive pulmonary disease (COPD) is a common, preventable, and treatable disease. The incidence of COPD is growing annually in China, and it is a significant and growing public health burden. Multivariate analysis showed that COPD was one of the independent risk factors for the occurrence of pulmonary embolism (PE), and the incidence of PE was significantly higher in COPD patients than in normal subjects. However, PE is often overlooked in patients with acute exacerbation of COPD (AECOPD) because there are many similarities in clinical symptoms between PE and AECOPD, which are difficult to distinguish, resulting in the failure of timely treatment and poor prognosis. Therefore, it is of great significance to understand the clinical manifestations, diagnosis, and treatment of COPD combined with PE for making a more accurate diagnosis, providing timely and effective treatment, and improving the prognosis of such patients.

简介：AbstractOver the last 20 years, it has become possible to use a precision medicine approach to the management of chronic obstructive pulmonary disease (COPD). Clinical and physiological features as well as a blood biomarker can be used to target treatments to patients most likely to benefit and avoid treatment in patients less likely to benefit. Future advances in a precision medicine approach to COPD will depend on more precise characterization of individual patients, possibly using quantitative imaging, new physiological techniques, novel biomarkers and genetic profiling. Precision medicine has led to significant improvements in the management of COPD and clinicians should use all available information to optimize the treatment of individual patients.

简介：AbstractThere is considerable epidemiological evidence indicating that air pollution has adverse effects on human health and is closely related to respiratory diseases, including chronic obstructive pulmonary disease (COPD). These effects, which can be divided into short- and long-term effects, can manifest as an exacerbation of existing symptoms, impaired lung function, and increased hospitalization and mortality rates. Long-term exposure to air with a high concentration of pollutants may also increase the incidence of COPD. The combined effects of different pollutants may become more complex in the future; hence, there is a need for more intensive research on specific at-risk populations, and formulating corresponding protective strategies is crucial. We aimed to review the epidemiological evidence on the effect of air pollution on COPD, the possible pathophysiological mechanisms underlying this effect, as well as protective measures against the effects of air pollutants in patients with COPD.

简介：AbstractChronic obstructive pulmonary disease (COPD), characterized by persistent and not fully reversible airflow restrictions, is currently one of the most widespread chronic lung diseases in the world. The most common symptoms of COPD are cough, expectoration, and exertional dyspnea. Although various strategies have been developed during the last few decades, current medical treatment for COPD only focuses on the relief of symptoms, and the reversal of lung function deterioration and improvement in patient’s quality of life are very limited. Consequently, development of novel effective therapeutic strategies for COPD is urgently needed. Stem cells were known to differentiate into a variety of cell types and used to regenerate lung parenchyma and airway structures. Stem cell therapy is a promising therapeutic strategy that has the potential to restore the lung function and improve the quality of life in patients with COPD. This review summarizes the current state of knowledge regarding the clinical research on the treatment of COPD with mesenchymal stem cells (MSCs) and aims to update the understanding of the role of MSCs in COPD treatment, which may be helpful for developing effective therapeutic strategies in clinical settings.

简介：AbstractChronic obstructive pulmonary disease (COPD) is a respiratory disease with a high incidence, mortality, and disability rate. Because there are few symptoms in the early stages of COPD, diagnosis and treatment are seriously insufficient. It is necessary to find effective clues for early COPD diagnosis and provide appropriate interventions. Several studies suggest that small airway disease is the earliest stage of COPD because it is correlated with subsequent development of airflow obstruction. However, there are currently no globally accepted criteria for defining early COPD. This study mainly introduced risk factors, definition, diagnosis, and treatment of early COPD from a new perspective.

简介：目的:观察推拿和呼吸体操治疗对缓解期慢性阻塞性肺病患者肺功能、呼吸困难、运动能力和生活质量的影响.方法:缓解期慢性阻塞性肺病患者66例,随机数字表法分为2组,推拿组(n=33)和对照组(n=33),治疗3个月.治疗前后进行呼吸困难、生活质量评分和肺功能、6min步行测试.结果:推拿组,肺功能观察指标显著改善;对照组,肺功能改善不明显.两种方法对生活质量均有提高,但推拿疗法优于呼吸体操.两种方法均能增加患者6min步行距离,均能改善呼吸困难,但两者差异无显著意义.结论:两种治疗方法显示对缓解期慢性阻塞性肺病患者呼吸困难、生活质量、运动耐受能力和肺功能有着较好的治疗效果,特别是推拿治疗对缓解期慢性阻塞性肺病的肺功能和生活质量的影响优于对照方法.

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简介：AbstractRespiratory viruses are major human pathogens that cause approximately 200 million pneumonia cases annually and induce various comorbidities with chronic obstructive pulmonary disease (COPD), resulting in significant health concerns and economic burdens. Clinical manifestations in respiratory viral infections and inflammations vary from asymptomatic, mild, to severe, depending on host immune cell responses to pathogens and interactions with airway epithelia. We critically review the activation, effector, and regulation of T cells in respiratory virus infections and chronic inflammations associated with COPD. Crosstalk among T cells, innate immune cells, and airway epithelial cells is discussed as essential parts of pathogenesis and protection in viral infections and COPD. We emphasize the specificity of peptide antigens and the functional heterogeneity of conventional CD4+ and CD8+ T cells to shed some light on potential cellular and molecular candidates for the future development of therapeutics and intervention against respiratory viral infections and inflammations.

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简介：AbstractBackground:The eosinophilic chronic obstructive pulmonary disease (COPD) is known to be more sensitive to corticosteroid. The sputum microbiome has been shown to affect COPD prognosis, but its role in acute exacerbations of eosinophilic COPD is unclear. This study aimed to investigate the dynamic changes of the airway microbiome in patients with acute exacerbations of eosinophilic COPD.Methods:Fifty-seven patients with acute exacerbations of COPD from the First Affiliated Hospital of Guangxi Medical University between June 2017 and June 2018 were divided into two groups. Patients with eosinophils ≥300 cells/μL in the peripheral venous blood were assigned to the eosinophilic group (Eos) and the rest to the non-eosinophilic group (Noneos). All patients received similar treatment including inhaled budesonide according to the guidelines. The induced sputum microbiome was analyzed on the 1st and 7th day of treatment using the 16S ribosomal RNA (rRNA) method. The levels of interleukin (IL)-6 and IL-8 were measured in the plasma and the sensitivity to corticosteroids was determined in isolated peripheral blood mononuclear cells. Quantitative data were compared between the two groups using the independent samples t test or Mann-Whitney U test. Categorical data were evaluated using Chi-squared test or Fisher’s exact test.Results:Twenty-six patients were classified into Eos group and 31 patients were classified into Noneos group. Prior to treatment, the alpha diversity (Shannon index) (2.65 ± 0.63 vs. 2.56 ± 0.54, t = 0.328, P = 0.747) and the structure of the sputum microbiome were similar in the Eos group and the Noneos group. After 7 days of treatment, alpha diversity increased in both groups, while the microbiome richness (Ace index) was significantly lower in the Eos group (561.87 ± 109.13 vs. 767.88 ± 148.48, t = -3.535, P = 0.002). At the same time, IL-6 (12.09 ± 2.85 pg/mL vs. 15.54 ± 2.45 pg/mL, t = -4.913, P < 0.001) and IL-8 (63.64 ± 21.69 pg/mL vs. 78.97 ± 17.13 pg/mL, t = -2.981, P = 0.004) decreased more significantly in the Eos group, and the percentages of inhibition of IL-8 at dexamethasone concentrations 10-8 to 10-6 mol/L were significantly higher in the Eos group than those in the Noneos group (all P < 0.05).Conclusions:The induced sputum microbiome richness decreased more significantly following treatment in the Eos patients compared to the Noneos patients. The lower plasma inflammatory factor levels and the higher percentage of inhibition of IL-8 might be due to higher corticosteroid sensitivity in Eos patients.

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简介：AbstractBackground:Due to airway remodeling and emphysematous destruction in the lung, the two classical clinical phenotypes of chronic obstructive pulmonary disease (COPD) are emphysema and bronchiolitis. The present study was designed to investigate the levels of small airway immunoglobulin A (IgA) in COPD with "emphysema phenotype." The study also evaluated the associations between the small airway IgA levels and the severity of disease by the extent of emphysema versus airflow limitation.Methods:Thirty patients (20 with COPD and ten healthy smokers) undergoing lung resection surgery for a solitary peripheral nodule were included. The study was conducted from January 2015 to December 2018 in the Shanxi Dayi Hospital. The presence of small airway IgA expression was determined in the lung by immunohistochemistry. In vivo, Wistar rats were exposed to silica by intratracheal instillation. Rats were sacrificed at 15 and 30 days after exposure of silica (n = 10 for each group). We also evaluated airway IgA from rats.Results:Small airway secretory IgA (sIgA), dimeric IgA (dIgA), and dIgA/sIgA of Global Initiative for Chronic Obstructive Lung Disease grade 1-2 COPD patients showed no difference compared with smoking control subjects (5.15±1.53 vs. 6.03±0.85; 1.94±0.66 vs. 1.67±0.04; 41.69±21.02 vs. 28.44±9.45, all P > 0.05). dIgA/sIgA level in the lung of COPD patients with emphysema showed higher levels than that of COPD patients without emphysema (51.89±24.81 vs. 31.49±9.28, P=0.03). The percentage of low-attenuation area below 950 Hounsfield units was positively correlated with dIgA/sIgA levels (r=0.45, P=0.047), but not associated with the severity of disease by spirometric measurements (forced expiratory volume in the first second %pred, P>0.05). Likewise, in the rat study, significant differences in sIgA, dIgA, dIgA/sIgA, mean linear intercept, mean alveoli number, and mean airway thickness of bronchioles (VV airway, all P < 0.01) were only observed between control rats and those exposed for 30 days. However, in the group exposed for 15 days, although the VV airway was higher than that in normal rats (27.61±2.26 vs. 20.39±1.99, P<0.01), there were no significant differences in IgA and emphysema parameters between the two groups (all P>0.05).Conclusion:Airway IgA concentrations in mild and moderate COPD patients are directly associated with the severity of COPD with "emphysema phenotype" preceding severe airway limitation. This finding suggests that small airway IgA might play an important role in the pathophysiology of COPD, especially emphysema phenotype.

简介：AbstractBackground:The incidence of chronic obstructive pulmonary disease (COPD) complicated with invasive pulmonary aspergillosis (IPA) has increased in the last two decades. The mechanism underpinning susceptibility to and high mortality of COPD complicated with IPA is unclear, and the role of T helper cells 17 (Th17 cells) in the compound disease remains unknown. Therefore, this study aimed to assess the function of Th17 cells in COPD combined with IPA.Methods:COPD, IPA, and COPD+IPA mouse models were established in male wild type C57/BL6 mice. The amounts of Th17 cells and retinoic acid-related orphan receptors γt (RORγt) were tested by flow cytometry. Then, serum interleukin (IL)-17 and IL-23 levels were detected by enzyme-linked immunosorbent assay (ELISA) in the control, COPD, IPA and COPD+IPA groups. In addition, COPD+IPA was induced in IL-17 knockout (KO) mice, for determining the role of Th17 cells in COPD+IPA.Results:Compared with the COPD group, the COPD+IPA group showed higher amounts of blood RORγt ([35.09 ± 16.12]% vs. [17.92 ± 4.91]%, P = 0.02) and serum IL-17 (17.96 ± 9.59 pg/mL vs. 8.05 ± 4.44 pg/mL, P = 0.02), but blood ([5.18 ± 1.09]% vs. [4.15 ± 0.87]%, P= 0.28) and lung levels of Th17 cells ([1.98 ± 0.83]% vs. [2.03 ± 0.98]%, P= 0.91), lung levels of RORγt ([9.58 ± 6.93]% vs. [9.63 ± 5.98]%, P = 0.49) and serum IL-23 (51.55 ± 27.82 pg/mL vs. 68.70 ± 15.20 pg/mL, P = 0.15) showed no significant differences. Compared with the IPA group, the COPD+IPA group displayed lower amounts of blood ([5.18 ± 1.09]% vs. [9.21 ± 3.56]%, P = 0.01) and lung Th17 cells ([1.98 ± 0.83]% vs. [6.29 ± 1.11]%, P = 0.01) and serum IL-23 (51.55 ± 27.82 pg/mL vs. 154.90 ± 64.60 pg/mL, P = 0.01) and IL-17 (17.96 ± 9.59 pg/mL vs. 39.81 ± 22.37 pg/mL, P = 0.02), while comparable blood ([35.09 ± 16.12]% vs. [29.86 ± 15.42]%, P = 0.25) and lung levels of RORγt ([9.58 ± 6.93]% vs. [15.10 ± 2.95]%, P = 0.18) were found in these two groups. Finally, Aspergillus load in IL-17 KO COPD+IPA mice was almost 2 times that of COPD+IPA mice (1,851,687.69 ± 944,480.43 vs. 892,958.10 ± 686,808.80, t= 2.32, P = 0.02).Conclusion:These findings indicate that Th17 cells might be involved in the pathogenesis of COPD combined with IPA, with IL-17 likely playing an antifungal role.

简介：AbstractPulmonary rehabilitation (PR) is a cornerstone management for chronic obstructive pulmonary disease (COPD). International respiratory societies defined PR is more than "just an exercise program" ; it is a comprehensive care delivered by a team of dedicated healthcare professionals with a strong emphasis on long-term health-enhancing Behaviors. However, "Uncertainty" exists with varied reasons for the political and geographical barriers of referral, uptake, attendance, and completion of PR in both primary and secondary care. Besides, COVID-19 pandemic has sparked many global controversies and challenges on pulmonary rehabilitation service delivery. Post-COVID-19 guidelines emphasize on integrated care rehabilitation for patients with COPD. Thus, this concise review intends to understand the gaps in United Kingdom healthcare policies, practices, and PR services resources. To date, there is no clear consensus on PR integrated care model pathway to address the unmet needs, measure the health and social care disparities; adds to the disease burden of COPD. Based on the culmination of evidence, this perspective offers a theoretical framework of PR integrated service model, a pathway to deliver high-value personalized care to patients with COPD.

简介：AbstractBackground:Fibrosis in the peripheral airways contributes to airflow limitation in patients with chronic obstructive pulmonary disease (COPD). However, the key proteins involved in its development are still poorly understood. Thus, we aimed to identify the differentially expressed proteins (DEPs) between smoker patients with and without COPD and elucidate the molecular mechanisms involved by investigating the effects of the identified biomarker candidate on lung fibroblasts.Methods:The potential DEPs were identified by isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomic analysis. The messenger RNA and protein levels of clusterin (CLU) in COPD patients and 12% cigarette smoke extract (CSE)-treated human bronchial epithelial cells were determined at the indicated time points. Furthermore, an in vitro COPD model was established via the administration of 8% CSE to normal human lung fibroblasts (NHLFs) at indicated time points. The effects of CSE treatment and CLU silencing on proliferation and activation of lung fibroblasts were analyzed.Results:A total of 144 DEPs were identified between COPD patients and normal smokers. The iTRAQ-based proteomics and bioinformatics analyses identified CLU as a serum biomarker candidate. We also discovered that CLU levels were significantly increased (P < 0.0001) in Global Initiative for Obstructive Lung Disease II, III, and IV patients and correlated (P < 0.0001) with forced expiratory volume in 1 s (R=-0.7705), residual volume (RV) (R = 0.6281), RV/total lung capacity (R = 0.5454), and computerized tomography emphysema (R = 0.7878). Similarly, CLU levels were significantly increased in CSE-treated cells at indicated time points (P < 0.0001). The CSE treatment significantly inhibited the proliferation, promoted the inflammatory response, differentiation of NHLFs, and collagen matrix deposition, and induced the apoptosis of NHLFs; however, these effects were partially reversed by CLU silencing.Conclusion:Our findings suggest that CLU may play significant roles during airway fibrosis in COPD by regulating lung fibroblast activation.

简介：AbstractChronic obstructive pulmonary disease (COPD) is a heterogeneous disease characteristic of small airway inflammation, obstruction, and emphysema. It is well known that spirometry alone cannot differentiate each separate component. Computed tomography (CT) is widely used to determine the extent of emphysema and small airway involvement in COPD. Compared with the pulmonary function test, small airway CT phenotypes can accurately reflect disease severity in patients with COPD, which is conducive to improving the prognosis of this disease. CT measurement of central airway morphology has been applied in clinical, epidemiologic, and genetic investigations as an inference of the presence and severity of small airway disease. This review will focus on presenting the current knowledge and methodologies in chest CT that aid in identifying discrete COPD phenotypes.

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