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:BACKGROUND:Little is known about the interactions between the lung microbiome and host response in chronic obstructive pulmonary disease (COPD). METHODS:We 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. RESULTS:Dysbiosis 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. CONCLUSIONS:Our 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.
| S-EPMC6555748 | biostudies-literature
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.
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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: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:Chronic Obstructive Pulmonary Disease (COPD) patient microbiome
| PRJEB46960 | ENA
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:Specific bacterial species are implicated in the pathogenesis of exacerbations of chronic obstructive pulmonary disease (COPD). However, recent studies of clinically stable COPD patients have demonstrated a greater diversity of airway microbiota, whose role in acute exacerbations is unclear. In this study, temporal changes in the airway microbiome before, at the onset of, and after an acute exacerbation were examined in 60 sputum samples collected from subjects enrolled in a longitudinal study of bacterial infection in COPD. Microbiome composition and predicted functions were examined using 16S rRNA-based culture-independent profiling methods. Shifts in the abundance (? 2-fold, P < 0.05) of many taxa at exacerbation and after treatment were observed. Microbiota members that were increased at exacerbation were primarily of the Proteobacteria phylum, including nontypical COPD pathogens. Changes in the bacterial composition after treatment for an exacerbation differed significantly among the therapy regimens clinically prescribed (antibiotics only, oral corticosteroids only, or both). Treatment with antibiotics alone primarily decreased the abundance of Proteobacteria, with the prolonged suppression of some microbiota members being observed. In contrast, treatment with corticosteroids alone led to enrichment for Proteobacteria and members of other phyla. Predicted metagenomes of particular microbiota members involved in these compositional shifts indicated exacerbation-associated loss of functions involved in the synthesis of antimicrobial and anti-inflammatory products, alongside enrichment in functions related to pathogen-elicited inflammation. These trends reversed upon clinical recovery. Further larger studies will be necessary to determine whether specific compositional or functional changes detected in the airway microbiome could be useful indicators of exacerbation development or outcome.
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Project description:BACKGROUND:The prevalence of disabilities is rising steadily, reflecting an aging population and an increasing burden of chronic conditions affecting quality of life. There are scant national data on the prevalence of disability among individuals with chronic obstructive pulmonary disease (COPD). The main objective was to estimate the prevalence of common disabilities among US-based individuals diagnosed with COPD. METHODS:Data from the BRFSS, a national telephone survey examining health-related behaviors in 2016-2017 were analyzed. The study population consisted of individuals with self-reported COPD (N = 38352 in 2016 and N = 35423 in 2017). The prevalence of disabilities in hearing, vision, cognition, mobility, and independent living were obtained and adjusted with sampling weights. Healthcare access measures were described by type of disability. RESULTS:Mobility disability had the highest prevalence of 45.9 (44.8-47.0) % in 2016 and 48.4 (47.3-49.5) % in 2017 among respondents with COPD. The prevalence of disabilities was highest among those 45-64 years old, except for hearing and cognition. Hearing disabilities were most prevalent among males with COPD while cognitive and mobility disabilities were most prevalent among females with COPD. While differences in the prevalence of disabilities were observed, access to health care was similar by disability type and age group among respondents. CONCLUSION:Contrary to expectation, the highest prevalence of disabilities was found not to be among those 65 years old and above. Further research is needed to explain this age-specific shift in the burden of disability, as long-term care planning and prevention support systems should be informed by the demographical patterns of disabilities among individuals with COPD.
| S-EPMC7046217 | biostudies-literature