Potential of Health and Demographic Surveillance System in Asthma and Chronic Obstructive Pulmonary Disease Microbiome Research.
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ABSTRACT:
SUBMITTER: Agarwal D
PROVIDER: S-EPMC5543077 | biostudies-other | 2017
REPOSITORIES: biostudies-other
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Project description:Bacterial infection of lung airways underlies some of the main complications of COPD, significantly impacting disease progression and outcome. Colonization by bacteria may further synergize, amplify, or trigger pathways of tissue damage started by cigarette smoke, contributing to the characteristic airway inflammation and alveolar destruction of COPD. We sought to elucidate the presence and types of lung bacterial populations in different stages of COPD, aimed at revealing important insights into the pathobiology of the disease. Sequencing of the bacterial small subunit ribosomal RNA gene in 55 well-characterized clinical lung samples, revealed the presence of Novosphingobium spp. (>2% abundance) in lungs of patients with GOLD 3-GOLD 4 COPD, cystic fibrosis and a subset of control individuals. Novosphingobium-specific quantitative PCR was concordant with the sequence data and high levels of Novosphingobium spp. were quantifiable in advanced COPD, but not from other disease stages. Using a mouse model of subacute lung injury due to inhalation of cigarette smoke, bronchoalveolar lavage neutrophil and macrophage counts were significantly higher in mice challenged intratracheally with N. panipatense compared to control mice (p<0.01). Frequencies of neutrophils and macrophages in lung tissue were increased in mice challenged with N. panipatense at room air compared to controls. However, we did not observe an interaction between N. panipatense and subacute cigarette smoke exposure in the mouse. In conclusion, Novosphingobium spp. are present in more severe COPD disease, and increase inflammation in a mouse model of smoke exposure.
| S-EPMC4207766 | biostudies-literature
Project description:Chronic respiratory diseases (CRDs) are an important factor of morbidity and mortality, accounting for approximately 6% of total deaths worldwide. The main CRDs are asthma and chronic obstructive pulmonary disease (COPD). These complex diseases have different triggers including allergens, pollutants, tobacco smoke, and other risk factors. It is important to highlight that although CRDs are incurable, various forms of treatment improve shortness of breath and quality of life. The search for tools that can ensure accurate diagnosis and treatment is crucial. MicroRNAs (miRNAs) are small non-coding RNAs and have been described as promising diagnostic and therapeutic biomarkers for CRDs. They are implicated in multiple processes of asthma and COPD, regulating pathways associated with inflammation, thereby showing that miRNAs are critical regulators of the immune response. Indeed, miRNAs have been found to be deregulated in several biofluids (sputum, bronchoalveolar lavage, and serum) and in both structural lung and immune cells of patients in comparison to healthy subjects, showing their potential role as biomarkers. Also, miRNAs play a part in the development or termination of histopathological changes and comorbidities, revealing the complexity of miRNA regulation and opening up new treatment possibilities. Finally, miRNAs have been proposed as prognostic tools in response to both conventional and biologic treatments for asthma or COPD, and miRNA-based treatment has emerged as a potential approach for clinical intervention in these respiratory diseases; however, this field is still in development. The present review applies a systems biology approach to the understanding of miRNA regulatory networks in asthma and COPD, summarizing their roles in pathophysiology, diagnosis, and treatment.
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Project description:RationaleBased on surface brushings and bronchoalveolar lavage fluid, Hilty and coworkers demonstrated microbiomes in the human lung characteristic of asthma and chronic obstructive pulmonary disease (COPD), which have now been confirmed by others.ObjectivesTo extend these findings to human lung tissue samples.MethodsDNA from lung tissue samples was obtained from nonsmokers (n = 8); smokers without COPD (n = 8); patients with very severe COPD (Global Initiative for COPD [GOLD] 4) (n = 8); and patients with cystic fibrosis (CF) (n = 8). The latter served as a positive control, with sterile water as a negative control. All bacterial community analyses were based on polymerase chain reaction amplifying 16S rRNA gene fragments. Total bacterial populations were measured by quantitative polymerase chain reaction and bacterial community composition was assessed by terminal restriction fragment length polymorphism analysis and pyrotag sequencing.Measurement and main resultsTotal bacterial populations within lung tissue were small (20-1,252 bacterial cells per 1,000 human cells) but greater in all four sample groups versus the negative control group (P < 0.001). Terminal restriction fragment length polymorphism analysis and sequencing distinguished three distinct bacterial community compositions: one common to the nonsmoker and smoker groups, a second to the GOLD 4 group, and the third to the CF-positive control group. Pyrotag sequencing identified greater than 1,400 unique bacterial sequences and showed an increase in the Firmicutes phylum in GOLD 4 patients versus all other groups (P < 0.003) attributable to an increase in the Lactobacillus genus (P < 0.0007).ConclusionsThere is a detectable bacterial community within human lung tissue that changes in patients with very severe COPD.
| S-EPMC3359894 | biostudies-literature
Project description:BackgroundLittle is known about the interactions between the lung microbiome and host response in chronic obstructive pulmonary disease (COPD).MethodsWe performed a longitudinal 16S ribosomal RNA gene-based microbiome survey on 101 sputum samples from 16 healthy subjects and 43 COPD patients, along with characterization of host sputum transcriptome and proteome in COPD patients.ResultsDysbiosis of sputum microbiome was observed with significantly increased relative abundance of Moraxella in COPD versus healthy subjects and during COPD exacerbations, and Haemophilus in COPD ex-smokers versus current smokers. Multivariate modeling on sputum microbiome, host transcriptome and proteome profiles revealed that significant associations between Moraxella and Haemophilus, host interferon and pro-inflammatory signaling pathways and neutrophilic inflammation predominated among airway host-microbiome interactions in COPD. While neutrophilia was positively correlated with Haemophilus, interferon signaling was more strongly linked to Moraxella. Moreover, while Haemophilus was significantly associated with host factors both in stable state and during exacerbations, Moraxella-associated host responses were primarily related to exacerbations.ConclusionsOur study highlights a significant airway host-microbiome interplay associated with COPD inflammation and exacerbations. These findings indicate that Haemophilus and Moraxella influence different components of host immune response in COPD, and that novel therapeutic strategies should consider targeting these bacteria and their associated host pathways in COPD.
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Project description:Diaphragm muscles in Chronic Obstructive Pulmonary Disease (COPD) patients undergo an adaptive fast to slow transformation that includes cellular adaptations. This project studies the signaling mechanisms responsible for this transformation. Keywords: other
2003-07-16 | GSE475 | GEO
Project description:Chronic Obstructive Pulmonary Disease (COPD) patient microbiome
| PRJEB46960 | ENA
Project description:We hypothesized that asthma/chronic obstructive pulmonary disease (COPD) might increase the risk of chronic otitis media (COM), as asthma or COPD affects other diseases. The aim of this research was to investigate whether the incidence of COM is affected by a diagnosis of asthma or COPD in patients compared to matched controls from the national health screening cohort. A COM group (n = 11,587) and a control group that was 1:4 matched for age, sex, income, and residence area (n = 46,348) were selected. The control group included participants who never received treatment for COM from Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2015. The crude and adjusted odds ratios (ORs) of previous asthma/COPD before the index date for COM were analyzed using conditional logistic regression. The analyses were stratified by age, sex, income, and region of residence. The period prevalence of asthma (17.5% vs. 14.3%, p < 0.001) and COPD (6.6% vs. 5.0%, p < 0.001) were significantly higher in the COM group than in the control group. In addition, the odds of asthma and COPD were significantly higher in the COM group than in the control group. Both asthma (adjusted OR 1.23, 95% confidence interval [CI] 1.16-1.31, p < 0.001) and COPD (adjusted OR 1.23, 95% CI 1.13-1.35, p < 0.001) increased the ORs for COM. This positive association between asthma/COPD and COM indicates that asthma/COPD might increase the incidence of COM.
| S-EPMC8913729 | biostudies-literature
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:Neutrophils play a central role in innate immunity, inflammation, and resolution. Unresolving neutrophilia features as a disrupted inflammatory process in the airways of patients with chronic obstructive pulmonary disease (COPD) and severe asthma. The extent to which this may be linked to disease pathobiology remains obscure and could be further confounded by indication of glucocorticoids or concomitant respiratory infections. The formation of neutrophil extracellular traps (NETs) represents a specialized host defense mechanism that entrap and eliminate invading microbes. NETs are web-like scaffolds of extracellular DNA in complex with histones and neutrophil granular proteins, such as myeloperoxidase and neutrophil elastase. Distinct from apoptosis, NET formation is an active form of cell death that could be triggered by various microbial, inflammatory, and endogenous or exogenous stimuli. NETs are reportedly enriched in neutrophil-dominant refractory lung diseases, such as COPD and severe asthma. Evidence for a pathogenic role for respiratory viruses (e.g., Rhinovirus), bacteria (e.g., Staphylococcus aureus) and fungi (e.g., Aspergillus fumigatus) in NET induction is emerging. Dysregulation of this process may exert localized NET burden and contribute to NETopathic lung inflammation. Disentangling the role of NETs in human health and disease offer unique opportunities for therapeutic modulation. The chemokine CXCR2 receptor regulates neutrophil activation and migration, and small molecule CXCR2 antagonists (e.g., AZD5069, danirixin) have been developed to selectively block neutrophilic inflammatory pathways. NET-stabilizing agents using CXCR2 antagonists are being investigated in proof-of-concept studies in patients with COPD to provide mechanistic insights. Clinical validation of this type could lead to novel therapeutics for multiple CXCR2-related NETopathologies. In this Review, we discuss the emerging role of NETs in the clinicopathobiology of COPD and severe asthma and provide an outlook on how novel NET-stabilizing therapies via CXCR2 blockade could be leveraged to disrupt NETopathic inflammation in disease-specific phenotypes.
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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