Transcriptomic Signature of Asthma-Chronic Obstructive Pulmonary Disease Overlap in Whole Blood.
Ontology highlight
ABSTRACT:
SUBMITTER: Saferali A
PROVIDER: S-EPMC7874396 | biostudies-literature | 2021 Feb
REPOSITORIES: biostudies-literature
Publications
Transcriptomic Signature of Asthma-Chronic Obstructive Pulmonary Disease Overlap in Whole Blood.
Saferali Aabida A Yun Jeong H JH Lee Sool S Chase Robert P RP Bowler Russell P RP Castaldi Peter J PJ Hersh Craig P CP
American journal of respiratory cell and molecular biology 20210201 2
Similar Datasets
Project description:BackgroundAsthma-COPD overlap (ACO) is a respiratory condition with more severe respiratory symptoms, poorer quality of life, and increased hospital admissions compared with asthma or COPD alone.ObjectivesEstimate asthma, chronic obstructive pulmonary disease (COPD), and ACO prevalence among workers by industry and occupation and assess physical and mental health status, healthcare utilization, among workers with ACO.MethodsThe 2014-2018 National Health Interview Survey (NHIS) data for working adults aged ≥18 years employed (sample n = 99,424) in the 12 months prior to the survey were analyzed. Age-adjusted ACO, COPD and asthma prevalence and prevalence ratios adjusted for age, sex, race and smoking status were estimated.ResultsDuring 2014-2018, of the estimated 166 million (annual average) US workers, age-adjusted asthma, COPD, and ACO prevalence was 6.9%, 4.0%, and 1.1%, respectively. ACO prevalence was highest among workers aged ≥65 years (2.0%), females (1.6%), current smokers (1.9%), those living below the federal poverty level (2.3%), and workers in the accommodation and food services (1.6%) industry and personal care and service (2.3%) occupations. Workers with ACO had more frequent (p < 0.05) physician office visits, emergency department visits; and were more likely to be in poorer mental health, obese, have more lost workdays, more bed days, and comorbidities compared to workers with asthma alone and workers with COPD alone.Conclusion: Higher ACO prevalence among worker groups and increased healthcare utilization underscores the need for early identification of asthma and COPD, assessment of potential workplace exposures, and implementation of tailored interventions to reduce ACO among working adults.
| S-EPMC10664241 | biostudies-literature
Project description:PurposeWe conducted a cohort study to clarify this relationship between asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) and pulmonary embolism (PE).MethodsFrom the National Health Insurance Research Database of Taiwan, we identified patients who had a diagnosis of asthma and a diagnosis of COPD (defined as ACOS) and concurrent treatment between January 1999 and December 2009 (ACOS cohort: n = 14,150; non-ACOS cohort: n = 55,876). Cox proportional hazards regression analysis was performed to determine the adjusted hazard ratios (aHRs) for PE of the ACOS cohort compared with the non-ACOS cohort.ResultsComparing the ACOS cohort with the non-ACOS cohort, the aHR of PE was 2.08 (95% confidence intervals [CIs]: 1.56-2.76). The risk of PE was higher in ACOS cohort than non-ACOS cohort, regardless of age, sex, comorbidity, inhaled corticosteroids (ICSs) and oral steroids (OSs) used. For ages ranging from 20 to 65 years, the aHR of PE was 2.53 (95% CI: 1.44-4.44) in the ACOS cohort. ACOS patients using ICSs (aHR: 1.97, 95% CI: 1.29-3.01) or OSs (aHR: 1.97, 95% CI: 1.46-2.65), the risk of PE was higher than in the non-ACOS cohort. The risk of PE increased with the number of outpatient visits and hospitalizations necessitated, ranging from 2.32 (95% CI: 1.54-3.52) in patients having 3-9 visits to 4.20 (95% CI: 2.74-6.44) for those having >9 visits.ConclusionsACOS is associated with increased risk of PE, particularly patients with a high frequency of AE-even in young adults or people without comorbidities.
| S-EPMC5017612 | biostudies-literature
Project description:BackgroundFeatures of asthma and chronic obstructive pulmonary disease (COPD) can coexist in the same patient, in a condition termed asthma- chronic obstructive pulmonary disease overlap (ACO). ACO is heterogeneous condition exhibiting various combinations of asthma and COPD features. No clinically acceptable experimental model of ACO has been established. We aimed to establish an animal model of ACO.MethodsWe generated two phenotypes of ACO by administering ovalbumin and porcine pancreatic elastase in combination, and papain. The proinflammatory cytokines and cell types in bronchoalveolar lavage fluid (BALF) were investigated, and lung function parameters were measured using the FlexiVent system.ResultsGreater airway inflammation was observed in the asthma and both ACO models, and emphysema was found in the COPD and both ACO models. The proportion of eosinophils in BALF was elevated in the asthma and ACO-a model. Type 2 inflammatory cytokine levels were highest in the ACO-a model, and the neutrophil gelatinase-associated lipocalin level was elevated in the asthma and ACO-a model. Of lung function parameters, compliance was greater in the COPD and ACO-b model, in which elastance was lower than in the asthma model. Airway resistance increased with the methacholine concentration in the asthma and both ACO models, but not in the control or COPD model.ConclusionWe established two murine models of ACO that exhibit features of asthma and COPD. We validated the clinical relevance of the ACO models based on changes in cytokine profiles and lung function. These models will be useful in further studies of the pathogenesis of, and therapeutic targets for ACO.
| S-EPMC9728005 | biostudies-literature
Project description:PurposeTo clarify the relationship between asthma-chronic obstructive pulmonary disease overlap syndrome (ACOS) and depression.MethodsWe identified 10,911 patients who received an ACOS diagnosis and concurrent treatment between January 2000 and December 2009. Subjects without ACOS were included in the non-ACOS cohort (n = 10,911). Cox proportional hazard regression analysis was performed to compare the risk of depression between the ACOS and non-ACOS cohorts.ResultsThe risk of depression was higher in the ACOS cohort than in the non-ACOS cohort (adjusted hazard ratios (aHRs) = 1.67, 95% confidence interval [CI] = 1.48-1.88). In the ACOS cohort, the aHRs for depression were [2.44 (95% CI = 1.45-4.11); 2.36 (95% CI = 1.58-3.52)] in patients [aged 20-39 years; without comorbidity]. In the ACOS cohort, the aHRs for depression were 1.70 (95% CI = 1.51-1.93) and 1.84 (95% CI = 1.55-2.19) in patients without inhaled corticosteroids (ICSs) and oral steroids (OSs) use, respectively. Moreover, the aHRs for the risk of depression were 1.16 (95% CI = 0.95-1.41) and 1.12 (95% CI = 0.96-1.29) in patients with ICSs and OSs use, respectively.ConclusionThe risk of depression is higher in ACOS patients, even in those without comorbidities or in young adults. The events of the depression were not significant difference in patients receiving the ICSs/OSs between the ACOS and the non-ACOS cohorts.
| S-EPMC5726738 | biostudies-literature
Project description:The debate about whether asthma and chronic obstructive pulmonary disease (COPD) are distinct clinical syndromes is not new; there is heightened interest in understanding the group of individuals with obstructive lung disease who seem to have elements of both conditions because recent studies have demonstrated increased risk for respiratory events and exacerbations. We describe the clinical characteristics of this subtype of disease and suggest 4 working definitions of individuals who would fall into the asthma-COPD overlap category. Understanding the mechanisms underlying these subtypes will hopefully lead into a better understanding of therapeutic strategies that can target specific pathobiologic pathways.
| S-EPMC4943670 | biostudies-literature
Project description:To profile airway and parenchyma transcriptomes in our mouse model of asthma chronic obstructive pulmonary disease overlap, we employed RNA-Seq (TruSeq Stranded mRNA sample preparation, NovaSeq 6000, 20 million 100 bp single reads) as a discovery tool to identify mRNAs of interest in the development of experimental asthma chronic obstructive pulmonary disease overlap. Experimental asthma: Some mice were sensitized and challenged intranasally with house dust mite (HDM) extract 5 days per week for 3 weeks. In other mice, this was HDM treatment 3 times/week from weeks 4-11. Controls received phosphate buffered saline (PBS). Experimental chronic obstructive pulmonary disease (COPD): Mice were exposed to cigarette smoke (CS) twice per day, 5 days per week for 8 weeks. Control mice were exposed to normal air (AIR). Experimental asthma-COPD overlap (ACO): Mice were sensitized and challenged intranasally with HDM or PBS. From weeks 4-11, mice were also exposed to CS or AIR. Treatment with dexamethasone (DEX): Separate groups of mice were treated with DEX during week 11. Lungs were excised, airway and parenchyma tissue were isolated through blunt dissection, and total RNA isolated.
2023-02-01 | GSE199853 | GEO
Project description:Background: This study examined the differences in the prevalence and clinical features of asthma-chronic obstructive pulmonary disease (COPD) overlap (ACO) with identical diagnostic criteria by race and ethnicity in two nationwide cohorts of COPD. Methods: We used data from the Korean COPD Subgroup Study (KOCOSS) and phase I of the US Genetic Epidemiology of COPD (COPDGene) study. We defined ACO by satisfying bronchodilator response (BDR) >15% and 400 ml and/or blood eosinophil count ≥300/μl. Results: The prevalences of ACO according to ethnicity were non-Hispanic white (NHW), 21.4%; African American (AA), 17.4%; and Asian, 23.8%. Asian patients with ACO were older, predominantly male, with fewer symptoms, more severe airflow limitation, and fewer comorbidities than NHW and AA patients. During 1-year follow-up, exacerbations occurred in 28.2, 22.0, and 48.4% of NHW, AA, and Asian patients with ACO, respectively. Compared to patients with non-ACO from the same racial group, the risk for exacerbation was significantly higher in NHW and Asian patients with ACO [adjusted incident rate ratio (aIRR), 1.17; 95% CI, 1.01-1.36, and aIRR, 1.37; 95% CI, 1.09-1.71 for NHW and Asian patients with ACO, respectively]. Inhaled corticosteroid (ICS) reduced the risk for future exacerbation in total patients with ACO but the effect was not significant in each racial group. Conclusions: The prevalence of ACO was similar in the two cohorts using the same diagnostic criteria. The risk for future exacerbation was significantly higher in ACO, and the use of ICS reduced the risk for exacerbation in total patients with ACO.
| S-EPMC8645561 | biostudies-literature
Project description:To understand the key characteristics of Asthma and Chronic Obstructive Pulmonary Disease Overlap Syndrome (ACOS) and to identify evidence gaps relating to the identification, treatment and management of ACOS patients.A structured literature review and 1-hour telephone interviews with specialist respiratory physicians were conducted (n=10; China, France, Germany, Japan and the USA).All 10 physicians used the term ACOS in clinical practice. ACOS was not clearly defined in the literature. Prevalence of ACOS among adult patients with COPD or asthma ranged from 12-55%. ACOS patients had severe disease, with increased exacerbations and hospitalisations compared to some asthma and COPD patients. ACOS represented a clinical challenge due to a lack of evidence-based guidelines distinguishing between asthma, COPD and ACOS. Published data quantifying ACOS costs were limited.There is a need for consensus evidence-based guidance to facilitate earlier diagnosis and to optimise the management of ACOS patients.
| S-EPMC4819878 | biostudies-other
Project description:BackgroundThe effects of asthma, chronic obstructive pulmonary disease (COPD), or asthma-COPD overlap (ACO) on coronavirus disease 2019 (COVID-19) remain unclear.ObjectiveWe aimed to investigate the effects of chronic obstructive airway diseases such as asthma, COPD, and ACO on COVID-19.MethodsIn total, 5625 hospitalized patients with COVID-19 were divided into asthma, COPD, ACO, and control groups. A multivariate logistic regression analysis was performed to identify factors affecting the COVID-19 mortality rate. To find out whether chronic obstructive airway diseases such as asthma, COPD, and ACO affect COVID-19 mortality, 1:4 matching was performed, except for the ACO group alone due to a small number of patients.ResultsThe mortality rates of asthma, COPD, and ACO groups were about 2.3, 4.8, and 5.5 times higher than that of the control group, respectively. Although not statistically significant, the survival probability tended to decrease (asthma, COPD, and combined groups of asthma and ACO, hazard ratio [HR]: 1.84, 1.31, and 1.89, respectively). The survival probability of the combined groups of COPD, ACO, and asthma and the combined groups of COPD and ACO was significantly lower than that of the matched control group (HR: 3.00 and 1.99, respectively).ConclusionCompared to patients with COVID-19 without chronic obstructive airway disease, patients with these comorbidities are more likely to require oxygen and mechanical ventilators and have a higher mortality rate, which can be considered when classifying and monitoring patients in the era of COVID-19. Therefore, further studies are needed to evaluate the effect of chronic obstructive airway disease, especially ACO, on COVID-19 mortality.
| S-EPMC9066077 | biostudies-literature
Project description:Asthma and COPD overlap (ACO) is characterized by patients presenting with persistent airflow limitation and features of both asthma and COPD. It is associated with a higher frequency and severity of exacerbations, a faster lung function decline, and a higher healthcare cost. Systemic inflammation in COPD and asthma is driven by type 1 T helper (Th1) and Th2 immune responses, respectively, both of which may contribute to airway remodeling in ACO. ACO-related biomarkers can be classified into four categories: neutrophil-mediated inflammation, Th2 cell responses, arachidonic acid-eicosanoids pathway, and metabolites. Gene-environment interactions are key contributors to the complexity of ACO and are regulated by epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs. Thus, this review focuses on the link between epigenetics and ACO, and outlines the following: (I) inheriting epigenotypes without change with environmental stimuli, or epigenetic changes in response to long-term exposure to inhaled particles plus intermittent exposure to specific allergens; (II) epigenetic markers distinguishing ACO from COPD and asthma; (III) potential epigenetic drugs that can reverse oxidative stress, glucocorticoid insensitivity, and cell injury. Improved understanding of the epigenetic regulations holds great value to give deeper insight into the mechanisms, and clarify their implications for biomedical research in ACO.
| S-EPMC9179497 | biostudies-literature