Interaction of Biochemical Processes between Chronic Obstructive Pulmonary Disease (COPD), Pulmonary Arterial Hypertension (PAH), and Coronavirus Disease 2019 (COVID-19).

Both pulmonary arterial hypertension (PAH) and chronic obstructive pulmonary disease (COPD) are risk factors for coronavirus disease 2019 (COVID-19). Patients with lung injury and altered pulmonary vascular anatomy or function are more susceptible to infections. The purpose of the study is to ascertain whether individuals with COPD or PAH are affected synergistically by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Data sources for the construction of a protein-protein interaction (PPI) network and the identification of differentially expressed genes (DEGs) included three RNA-seq datasets from the GEO database (GSE147507, GSE106986, and GSE15197). Then, relationships between miRNAs, common DEGs, and transcription factor (TF) genes were discovered. Functional analysis using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and other databases, as well as the forecasting of antiviral medications for COPD and PAH patients infected with SARS-CoV-2, were also performed. Eleven common DEGs were found in the three datasets, and their biological functions were primarily enriched in the control of protein modification processes, particularly phosphorylation. Growth factor receptor binding reflects molecular function. KEGG analysis indicated that co-DEGs mainly activate Ras, and PI3K-Akt signaling pathways and act on focal adhesions. NFKB1 interacted with HSA-miR-942 in the TF-miRNA-DEGs synergistic regulatory network. Acetaminophen is considered an effective drug candidate. There are some connections between COPD and PAH and the development of COVID-19. This research could aid in developing COVID-19 vaccines and medication candidates that would work well as COVID-19 therapies.

An alternative mechanism for skeletal muscle dysfunction in long-term post-viral lung disease.

Chronic lung disease is often accompanied by disabling extrapulmonary symptoms, notably skeletal muscle dysfunction and atrophy. Moreover, the severity of respiratory symptoms correlates with decreased muscle mass and in turn lowered physical activity and survival rates. Previous models of muscle atrophy in chronic lung disease often modeled chronic obstructive pulmonary disease (COPD) and relied on cigarette smoke exposure and LPS stimulation, but these conditions independently affect skeletal muscle even without accompanying lung disease. Moreover, there is an emerging and pressing need to understand the extrapulmonary manifestations of long-term post-viral lung disease (PVLD) as found in COVID-19. Here, we examine the development of skeletal muscle dysfunction in the setting of chronic pulmonary disease caused by infection due to the natural pathogen Sendai virus using a mouse model of PVLD. We identify a significant decrease in myofiber size when PVLD is maximal at 49 days after infection. We find no change in the relative types of myofibers, but the greatest decrease in fiber size is localized to fast-twitch-type IIB myofibers based on myosin heavy chain immunostaining. Remarkably, all biomarkers of myocyte protein synthesis and degradation (total RNA, ribosomal abundance, and ubiquitin-proteasome expression) were stable throughout the acute infectious illness and chronic post-viral disease process. Together, the results demonstrate a distinct pattern of skeletal muscle dysfunction in a mouse model of long-term PVLD. The findings thereby provide new insights into prolonged limitations in exercise capacity in patients with chronic lung disease after viral infections and perhaps other types of lung injury.NEW & NOTEWORTHY Our study used a mouse model of post-viral lung disease to study the impact of chronic lung disease on skeletal muscle. The model reveals a decrease in myofiber size that is selective for specific types of myofibers and an alternative mechanism for muscle atrophy that might be independent of the usual markers of protein synthesis and degradation. The findings provide a basis for new therapeutic strategies to correct skeletal muscle dysfunction in chronic respiratory disease.

First booster dose uptake of COVID-19 vaccine and disease-related factors in chronic obstructive pulmonary disease-a cross-sectional survey in Hungary.

BACKGROUND: In chronic obstructive pulmonary disease (COPD), uptake of the coronavirus disease 2019 (COVID-19) booster vaccine is important, as they are more likely to develop serious complications. Our aim was to investigate the uptake rate of first booster vaccination against COVID-19 among COPD patients and to identify other related factors of vaccine uptake. METHODS: We conducted a multicenter survey of COPD patients in Hungary by region: eastern, western and central ones from 15 November 2021. Respiratory function test results, anthropometric data and vaccination status were recorded for 1,510 randomly selected patients over 35 years of age. Multiple logistic regression analysis was used to determine factors associated with uptake of COVID-19 first booster dose vaccines. RESULTS: The average age was 67 [61-72] years, for men it was: 67 [62-73] and 66 [60-72] years for women, with a sample of 47.95% men and 52.05% women. The uptake rate of the COVID-19 first booster vaccine during the study period was 62.45%. Comparing patients who received the 3rd vaccine with those who did not receive the 3rd vaccine, the difference was significant in quality of life: COPD Assessment Test (CAT): 16 [11-21] vs. 14 [10-19], P<0.001, modified Medical Research Council (mMRC) dyspnea scale: 2 [2-2] vs. 2 [1-2], P=0.01 and in the number of moderate exacerbations: 1 [0-1] vs. 0 [0-1], P=0.04. In addition, who did not take the third vaccination significantly more people were hospitalized for acute severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (16 vs. 0, P<0.001) and almost the same proportion (n=14) required pulmonary outpatient rehabilitation for post-COVID symptoms. The factors that were most associated with higher COVID-19 vaccine first booster dose uptake were older age [odds ratio (OR): 1.06; 95% confidence interval (CI): 1.04-1.08], male gender (OR: 0.74; 95% CI: 0.57-0.96), absence of previous COVID-19 infection (OR: 0.34; 95% CI: 0.23-0.51). CONCLUSIONS: The uptake rate of the COVID-19 booster vaccine among COPD patients in Hungary is lower than the target, and is associated with disease-related factors, and age, sex, previous COVID infection. The global COVID-19 vaccination target is 70% and 100% for elderly, vulnerable patients. Highlighting the importance of taking booster vaccine(s) should be a priority for health workers.

Cough Assessment and Management in Pulmonary Rehabilitation- A Canadian Survey.

Pulmonary rehabilitation is a cornerstone intervention for controlling respiratory symptoms in people with chronic respiratory diseases. Chronic cough affects up to 90% of people with chronic respiratory diseases, however, it is currently unknown whether chronic cough is assessed and/or managed in pulmonary rehabilitation. This study aimed to determine if and how chronic cough is assessed and managed in pulmonary rehabilitation. This was a cross-sectional study. Pulmonary rehabilitation programs in Canada were identified via online websites. A representative from each program was invited to complete an online survey including the following topics: program demographics, assessment and management practices, and barriers and facilitators. Of 133 programs contacted, 31 returned a completed survey (23% response rate). Approximately half (52%) of respondents reported enrolling patients with chronic cough. Of those, 45% reported assessing and 62% reported intervening in chronic cough. Inadequate knowledge of assessment and management techniques was commonly identified to be a barrier and increased education was suggested as a possible facilitator. Based on pulmonary rehabilitation programs that responded to our survey, chronic cough is a prevalent symptom; however, it is scarcely assessed and managed. A need for structured education and the use of standardised strategies were reported as facilitators to the assessment and management of chronic cough in pulmonary rehabilitation.

Expanding role of CXCR2 and therapeutic potential of CXCR2 antagonists in inflammatory diseases and cancers.

C-X-C motif chemokine receptor 2 (CXCR2) is G protein-coupled receptor (GPCR) and plays important roles in various inflammatory diseases and cancers, including chronic obstructive pulmonary disease (COPD), atherosclerosis, asthma, and pancreatic cancer. Upregulation of CXCR2 is closely associated with the migration of neutrophils and monocytes. To date, many small-molecule CXCR2 antagonists have entered clinical trials, showing favorable safety and therapeutic effects. Hence, we provide an overview containing the discovery history, protein structure, signaling pathways, biological functions, structure-activity relationships and clinical significance of CXCR2 antagonists in inflammatory diseases and cancers. According to the latest development and recent clinical progress of CXCR2 small molecule antagonists, we speculated that CXCR2 can be used as a biomarker and a new target for diabetes and that CXCR2 antagonists may also attenuate lung injury in coronavirus disease 2019 (COVID-19).

COVID-19 vaccination coverage in patients with chronic obstructive pulmonary disease - A cross-sectional study in Hungary.

INTRODUCTION: Coronavirus infection is a particular risk for patients with chronic obstructive pulmonary disease (COPD), because they are much more likely to become severely ill due to oxygen supply problems. Primary prevention, including COVID-19 vaccination is of paramount importance in this disease group. The aim of our study was to assess COVID-19 vaccination coverage in COPD patients during the first vaccination campaign of the COVID-19 pandemic. METHODS: A cross-sectional observational study (CHANCE) has been conducted in COPD patients in the eastern, western and central regions of Hungary from 15th November 2021. The anthropometric, respiratory function test results and vaccination status of 1,511 randomly selected patients were recorded who were aged 35 years and older. RESULTS: The median age was 67 (61-72) years, for men: 67 (62-73) and for women: 66 (60-72) years, with 47.98 % men and 52.02 % women in our sample. The prevalence of vaccination coverage for the first COVID-19 vaccine dose was 88.62 %, whereas 86.57 % of the patients received the second vaccine dose. When unvaccinated (n = 172) and double vaccinated (n = 1308) patients were compared, the difference was significant both in quality of life (CAT: 17 (12-23) vs 14 (10-19); p < 0.001) and severity of dyspnea (mMRC: 2 (2-2) vs 2 (1-2); p = 0.048). The COVID-19 infection rate between double vaccinated and unvaccinated patients was 1.61 % vs 22.67 %; p < 0.001 six months after vaccination. The difference between unvaccinated and vaccinated patients was significant (8.14 % vs 0.08 %; p < 0.001) among those with acute COVID-19 infection hospitalized. In terms of post-COVID symptoms, single or double vaccinated patients had significantly fewer outpatient hospital admissions than unvaccinated patients (7.56 vs 0 %; p < 0.001). CONCLUSION: The COVID-19 vaccination coverage was satisfactory in our sample. The uptake of COVID-19 vaccines by patients with COPD is of utmost importance because they are much more likely to develop severe complications.

The impact of facemask on patients with COPD: A systematic review and meta-analysis.

Background: Since the emergence of COVID-19, mandatory facemask wearing has been implemented around the world to prevent viral transmission, however, the impact of wearing facemasks on patients with COPD was unclear. Methods: The current study undertakes a systematic review and meta-analysis of a comprehensive literature retrieval from six databases, based on the pre-determined eligibility criteria, irrespective of language. The risk of bias was assessed using an established instrument. We primarily focused on analyzing ETCO2, SpO2, and heart and respiratory rates, and also considered the impacts on physiological and exercise performance. A descriptive summary of the data and possible meta-analysis was performed. Forest plots were generated to pool estimates based on each of the study outcomes. Results: Of the 3,751 publications considered, six publications were selected for a systematic review and two publications were included for meta-analysis, however, the quality of these six studies was relatively low overall. In the case of inactivity, the facemask wearing COPD cohort had higher respiratory rates than that of the non-facemask wearing cohort (MD = 1.00 and 95% CI 0.47-1.53, P < 0.05). There was no significant difference in ETCO2 (MD = 0.10 and 95% CI -1.57-1.78, P > 0.05) and heart rate (MD = 0.40 and 95% CI -3.59-4.39, P > 0.05) nor SpO2 (MD = -0.40 and 95% CI -0.84-0.04, P > 0.05) between the COPD patients with and without facemasks. Furthermore, it was observed that the only significant differences between the COPD patients with and without facemasks undertaking different activities were FEV1 (%) (MD = 3.84 and 95% CI 0.14-7.54, P < 0.05), FEV1/FVC (%) (MD = 3.25 and 95% CI 0.71-5.79, P < 0.05), and blood lactate (MD = -0.90 and 95% CI -1.73 to -0.07, P < 0.05). Conclusion: Wearing facemasks decreased the exercise performance of patients with COPD, however, it had minimal impact on physiological indexes. Further investigations will be performed on the high-quality data from randomized control studies. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=326265, identifier: CRD42022326265.

Metabolomics of Respiratory Diseases.

Metabolomics is an expanding field of systems biology that is gaining significant attention in respiratory research. As a unique approach to understanding and diagnosing diseases, metabolomics provides a snapshot of all metabolites present in biological samples such as exhaled breath condensate, bronchoalveolar lavage, plasma, serum, urine, and other specimens that may be obtained from patients with respiratory diseases. In this article, we review the rapidly expanding field of metabolomics in its application to respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD), pneumonia, and acute lung injury, along with its more severe form, adult respiratory disease syndrome. We also discuss the potential applications of metabolomics for monitoring exposure to aerosolized occupational and environmental materials. With the latest advances in our understanding of the microbiome, we discuss microbiome-derived metabolites that arise from the gut and lung in asthma and COPD that have mechanistic implications for these diseases. Recent literature has suggested that metabolomics analysis using nuclear magnetic resonance (NMR) and mass spectrometry (MS) approaches may provide clinicians with the opportunity to identify new biomarkers that may predict progression to more severe diseases which may be fatal for many patients each year.

Lung Spatial Profiling Reveals a T Cell Signature in COPD Patients with Fatal SARS-CoV-2 Infection.

People with pre-existing lung diseases such as chronic obstructive pulmonary disease (COPD) are more likely to get very sick from SARS-CoV-2 disease 2019 (COVID-19). Still, an interrogation of the immune response to COVID-19 infection, spatially throughout the lung structure, is lacking in patients with COPD. For this study, we characterized the immune microenvironment of the lung parenchyma, airways, and vessels of never- and ever-smokers with or without COPD, all of whom died of COVID-19, using spatial transcriptomic and proteomic profiling. The parenchyma, airways, and vessels of COPD patients, compared to control lungs had (1) significant enrichment for lung-resident CD45RO+ memory CD4+ T cells; (2) downregulation of genes associated with T cell antigen priming and memory T cell differentiation; and (3) higher expression of proteins associated with SARS-CoV-2 entry and primary receptor ubiquitously across the ROIs and in particular the lung parenchyma, despite similar SARS-CoV-2 structural gene expression levels. In conclusion, the lung parenchyma, airways, and vessels of COPD patients have increased T-lymphocytes with a blunted memory CD4 T cell response and a more invasive SARS-CoV-2 infection pattern and may underlie the higher death toll observed with COVID-19.

Emerging evidence for non-pharmacologic interventions in reducing the burden of respiratory illnesses.

The global pandemic caused by SARS-CoV-2 (COVID-19) has led to significant morbidity and mortality, and unprecedented economic and health system disruption. Non-pharmacologic interventions (NPIs) such as masking and physical distancing have formed the underpinnings of COVID-19 infection control strategies. Concomitantly, numerous jurisdictions have seen a decrease in hospitalizations for non-COVID-19 respiratory illnesses (NCRIs) such as asthma, community-acquired pneumonia, influenza, and chronic obstructive pulmonary disease relative to pre-pandemic levels. These associations give rise to a number of testable hypotheses regarding the efficacy of NPIs in reducing the substantial burden of NCRIs. Here, we review emerging perspectives on the role of NPIs in NCRI prevention with the ultimate goal of informing future research and public policy development as we move into what may be the endemic phase of the COVID-19 pandemic.

Grape Phytochemicals and Vitamin D in the Alleviation of Lung Disorders.

BACKGROUND: Typical lung diseases are pneumonia, asthma, sleep apnea syndrome (SA), interstitial pneumonia (IP), lung cancer, and chronic obstructive pulmonary disease (COPD). Coronavirus disease 2019 (COVID-19) is a type of viral pneumonia. Many researchers have reported that phytochemicals (chemical compounds produced by plants) and vitamin D are useful in stimulating our immunity. This review discusses the alleviation of lung diseases by grape phytochemicals and vitamin D. DISCUSSION: Pneumonia is an acute inflammation caused by the infection of pathogens; the worst case is a fatal cytokine storm in the lung. In asthma, allergens, tobacco smoke, or air pollution may cause seizures. Lung diseases caused by lung fibrosis may manifest chronic inflammation, progress into alveolar fibrosis, and cause respiratory malfunction. SA is a lifestyle disease related to obesity and metabolic syndrome. To alleviate these symptoms, changing the eating habit is one of the strategies. Improvement in the daily lifestyle reduces the risk of lung cancer. Self-management, including nutritional management and exercise, is very important for COPD patients in addition to pharmacotherapy. CONCLUSION: The intake of grape phytochemicals and vitamin D prevents the progress of lung diseases. Both phytochemicals and vitamin D prevent the production of proinflammatory cytokine, TNF-α, that is responsible for inflammation and lung diseases. Daily intake of grape phytochemicals is important. The optimum vitamin D level in serum is > 30 ng/mL. For the prevention of lung diseases, upregulating immunity and maintaining good gut microbiota are important because gut microbiota change depending on what we eat.

BPM Support for Patient-Centred Clinical Pathways in Chronic Diseases.

Epidemiological trends over the past decade show a significant worldwide increase in the burden of chronic diseases. At the same time, the human resources of health care are becoming increasingly scarce and expensive. One of the management concepts that can help in solving this problem is business process management (BPM). The results of research conducted in the healthcare sector thus far prove that BPM is an effective tool for optimizing clinical processes, as it allows for the ongoing automatic tracking of key health parameters of an individual patient without the need to involve medical personnel. The aim of this article is to present and evaluate the redesign of diagnostic and therapeutic processes enabling the patient-centric organization of therapy thanks to the use of new telemedicine techniques and elements of hyperautomation. By using an illustrative case study of one of the most common chronic diseases, Chronic Obstructive Pulmonary Disease (COPD), we discuss the use of clinical pathways (CPs) prepared on the basis of the current version of the Global Initiative for Chronic Obstructive Lung Disease (GOLD) as a communication tool between healthcare professionals, the patient and his or her caregivers, as well as the method of identifying and verifying new knowledge generated on an ongoing basis in diagnostic and therapeutic processes. We also show how conducting comprehensive, patient-focused primary health care relieves the health care system, and at the same time, thanks to the use of patient engagement and elements of artificial intelligence (predictive analyses), reduces the significant clinical risk of therapy.

The Role of Epithelial Damage in the Pulmonary Immune Response.

Pulmonary epithelial cells are widely considered to be the first line of defence in the lung and are responsible for coordinating the innate immune response to injury and subsequent repair. Consequently, epithelial cells communicate with multiple cell types including immune cells and fibroblasts to promote acute inflammation and normal wound healing in response to damage. However, aberrant epithelial cell death and damage are hallmarks of pulmonary disease, with necrotic cell death and cellular senescence contributing to disease pathogenesis in numerous respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and coronavirus disease (COVID)-19. In this review, we summarise the literature that demonstrates that epithelial damage plays a pivotal role in the dysregulation of the immune response leading to tissue destruction and abnormal remodelling in several chronic diseases. Specifically, we highlight the role of epithelial-derived damage-associated molecular patterns (DAMPs) and senescence in shaping the immune response and assess their contribution to inflammatory and fibrotic signalling pathways in the lung.

The History and Mystery of Alveolar Epithelial Type II Cells: Focus on Their Physiologic and Pathologic Role in Lung.

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air-liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.

Ageing mechanisms that contribute to tissue remodeling in lung disease.

Age is a major risk factor for chronic respiratory diseases such as idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD) and certain phenotypes of asthma. The recent COVID-19 pandemic also highlights the increased susceptibility of the elderly to acute respiratory distress syndrome (ARDS), a diffuse inflammatory lung injury with often long-term effects (ie parenchymal fibrosis). Collectively, these lung conditions are characterized by a pathogenic reparative process that, rather than restoring organ function, contributes to structural and functional tissue decline. In the ageing lung, the homeostatic control of wound healing following challenge or injury has an increased likelihood of being perturbed, increasing susceptibility to disease. This loss of fidelity is a consequence of a diverse range of underlying ageing mechanisms including senescence, mitochondrial dysfunction, proteostatic stress and diminished autophagy that occur within the lung, as well as in other tissues, organs and systems of the body. These ageing pathways are highly interconnected, involving localized and systemic increases in inflammatory mediators and damage associated molecular patterns (DAMPs); along with corresponding changes in immune cell function, metabolism and composition of the pulmonary and gut microbiomes. Here we comprehensively review the roles of ageing mechanisms in the tissue remodeling of lung disease.

Development of potent and selective Cathepsin C inhibitors free of aortic binding liability by application of a conformational restriction strategy.

Cathepsin C plays a key role in the activation of several degradative enzymes linked to tissue destruction in chronic inflammatory and autoimmune diseases. Therefore, Cathepsin C inhibitors could potentially be effective therapeutics for the treatment of diseases such as chronic obstructive pulmonary disease (COPD) or acute respiratory distress syndrome (ARDS). In our efforts towards the development of a novel series of Cathepsin C inhibitors, we started working around AZD5248 (1), an α-amino acid based scaffold having potential liability of aortic binding. A novel series of amidoacetonitrile based Cathepsin C inhibitors were developed by the application of a conformational restriction strategy on 1. In particular, this work led to the development of a potent and selective Cathepsin C inhibitor 3p, free of aortic binding liability.

Assessment of the Association of COPD and Asthma with In-Hospital Mortality in Patients with COVID-19. A Systematic Review, Meta-Analysis, and Meta-Regression Analysis.

Together, chronic obstructive pulmonary disease (COPD) and asthma account for the most common non-infectious respiratory pathologies. Conflicting preliminary studies have shown varied effect for COPD and asthma as prognostic factors for mortality in coronavirus disease 2019 (COVID-19). The aim of this study was to explore the association of COPD and asthma with in-hospital mortality in patients with COVID-19 by systematically reviewing and synthesizing with a meta-analysis the available observational studies. MEDLINE, Scopus, and medRxiv databases were reviewed. A random-effects model meta-analysis was used, and I-square was utilized to assess for heterogeneity. In-hospital mortality was defined as the primary endpoint. Sensitivity and meta-regression analyses were performed. Thirty studies with 21,309 patients were included in this meta-analysis (1465 with COPD and 633 with asthma). Hospitalized COVID-19 patients with COPD had higher risk of death compared to those without COPD (OR: 2.29; 95% CI: 1.79-2.93; I2 59.6%). No significant difference in in-hospital mortality was seen in patients with and without asthma (OR: 0.87; 95% CI: 0.68-1.10; I2 0.0%). The likelihood of death was significantly higher in patients with COPD that were hospitalized with COVID-19 compared to patients without COPD. Further studies are needed to assess whether this association is independent or not. No significant difference was demonstrated in COVID-19-related mortality between patients with and without asthma.

Electronic Cigarette Aerosol Is Cytotoxic and Increases ACE2 Expression on Human Airway Epithelial Cells: Implications for SARS-CoV-2 (COVID-19).

Tobacco smoking has emerged as a risk factor for increasing the susceptibility to infection from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) via increased expression of angiotensin-converting enzyme-2 (ACE2) in the lung, linked to coronavirus disease 2019 (COVID-19) development. Given the modifiable nature of electronic cigarettes and the delivery of high concentrations of nicotine, we investigate whether electronic cigarette vaping has the potential to increase susceptibility to SARS-CoV-2 infection. We exposed BEAS-2B cells (bronchial epithelium transformed with Ad12-SV40 2B) and primary small airway epithelial cells (SAECs) to electronic cigarette aerosol condensates produced from propylene glycol/vegetable glycerin or commercially bought e-liquid (±added nicotine) and cigarette smoke extract to investigate if electronic cigarette exposure, like cigarette smoke, increases the expression of ACE2 in lung epithelial cells. In BEAS-2B cells, cytotoxicity (CCK-8), membrane integrity (LDH), and ACE2 protein expression (immunofluorescence) were measured for both 4- and 24 h treatments in BEAS-2B cells and 4 h in SAECs; ACE2 gene expression was measured using quantitative polymerase chain reaction (qPCR) for 4 h treatment in BEAS-2B cells. Nicotine-free condensates and higher concentrations of nicotine-containing condensates were cytotoxic to BEAS-2B cells. Higher LDH release and reduced membrane integrity were seen in BEAS-2B cells treated for 24 h with higher concentrations of nicotine-containing condensates. ACE2 protein expression was observably increased in all treatments compared to cell controls, particularly for 24 h exposures. ACE2 gene expression was significantly increased in cells exposed to the locally bought e-liquid condensate with high nicotine concentration and cigarette smoke extract compared with cell controls. Our study suggests that vaping alone and smoking alone can result in an increase in lung ACE2 expression. Vaping and smoking are avoidable risk factors for COVID-19, which, if avoided, could help reduce the number of COVID-19 cases and the severity of the disease. This is the first study to utilize electronic cigarette aerosol condensates, novel and developed in our laboratory, for investigating ACE2 expression in human airway epithelial cells.

Medication adherence among patients with chronic obstructive pulmonary disease treated in a primary general hospital during the COVID-19 pandemic.

BACKGROUND: The objective of this study was to investigate medication adherence and the associated influencing factors in patients with chronic obstructive pulmonary disease (COPD) who were treated in a primary general hospital in Shanghai China during the 2019 novel coronavirus (COVID-19) pandemic. METHODS: From March to April 2020, all of the COPD patients treated in our department in the last 7 years were interviewed by telephone. The basic patient data and each questionnaire item were collected, and influencing factors were analyzed by the Chi-square test, U test, and univariate and multivariate logistic regression analyses. RESULTS: A total of 191 patients with COPD were queried, and 84 (44.0%) valid questionnaires were obtained. Among them, individuals with group B symptoms were most represented (45.2%); 53.6% had Medical Research Council (MRC) dyspnea levels of 2 or above. Chronic obstructive pulmonary disease assessment test (CAT) had an average of 9 [3, 13], and 52.4% of patients used two-drug combination therapy. Medication adherence was both good in ordinary times and over the past 2 months of the pandemic, and 88.8% of patients had no acute exacerbation during the pandemic. The CAT scores of male patients <70 years old, and patients with general outpatient follow-up and regular gargling were reduced (P<0.05). Drug combination and doctor's supervision were favorable factors affecting medication adherence during the 2 months of the pandemic, while possible depression was an unfavorable factor (P<0.05). CONCLUSIONS: During the pandemic, medication adherence in patients with COPD was similar to that in regular times, and was significantly related to drug combination, doctor's supervision, and accompanying mood disorders. An effective way to improve patient adherence and disease control could be strengthening follow-up education and diagnosing and treating depression and other complications.