Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Más filtros

Banco de datos
Tipo del documento
País de afiliación
Intervalo de año de publicación
1.
Thorax ; 71(9): 795-803, 2016 09.
Artículo en Inglés | MEDLINE | ID: mdl-27146202

RESUMEN

RATIONALE: The role bacteria play in the progression of COPD has increasingly been highlighted in recent years. However, the microbial community complexity in the lower airways of patients with COPD is poorly characterised. OBJECTIVES: To compare the lower airway microbiota in patients with COPD, smokers and non-smokers. METHODS: Bronchial wash samples from adults with COPD (n=18), smokers with no airways disease (n=8) and healthy individuals (n=11) were analysed by extended-culture and culture-independent Illumina MiSeq sequencing. We determined aerobic and anaerobic microbiota load and evaluated differences in bacteria associated with the three cohorts. Culture-independent analysis was used to determine differences in microbiota between comparison groups including taxonomic richness, diversity, relative abundance, 'core' microbiota and co-occurrence. MEASUREMENT AND MAIN RESULTS: Extended-culture showed no difference in total load of aerobic and anaerobic bacteria between the three cohorts. Culture-independent analysis revealed that the prevalence of members of Pseudomonas spp. was greater in the lower airways of patients with COPD; however, the majority of the sequence reads for this taxa were attributed to three patients. Furthermore, members of Bacteroidetes, such as Prevotella spp., were observed to be greater in the 'healthy' comparison groups. Community diversity (α and ß) was significantly less in COPD compared with healthy groups. Co-occurrence of bacterial taxa and the observation of a putative 'core' community within the lower airways were also observed. CONCLUSIONS: Microbial community composition in the lower airways of patients with COPD is significantly different to that found in smokers and non-smokers, indicating that a component of the disease is associated with changes in microbiological status.


Asunto(s)
Bacterias/aislamiento & purificación , Microbiota , Enfermedad Pulmonar Obstructiva Crónica/microbiología , Fumar , Adulto , Anciano , Bacterias/clasificación , Carga Bacteriana , Lavado Broncoalveolar , Líquido del Lavado Bronquioalveolar/microbiología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Filogenia , Manejo de Especímenes/métodos , Esputo/microbiología
2.
J Cyst Fibros ; 21(5): 837-843, 2022 09.
Artículo en Inglés | MEDLINE | ID: mdl-35764510

RESUMEN

BACKGROUND: Cystic Fibrosis (CF) has prominent gastrointestinal and pancreatic manifestations. The aim of this study was to determine the effect of Cystic fibrosis transmembrane conductance regulator (CFTR) modulation on, gastrointestinal inflammation, pancreatic function and gut microbiota composition in people with cystic fibrosis (CF) and the G551D-CFTR mutation. METHODS: Fourteen adult patients with the G551D-CFTR mutation were assessed clinically at baseline and for up to 1 year after treatment with ivacaftor. The change in gut inflammatory markers (calprotectin and lactoferrin), exocrine pancreatic status and gut microbiota composition and structure were assessed in stool samples. RESULTS: There was no significant change in faecal calprotectin nor lactoferrin in patients with treatment while all patients remained severely pancreatic insufficient. There was no significant change in gut microbiota diversity and richness following treatment. CONCLUSION: There was no significant change in gut inflammation after partial restoration of CFTR function with ivacaftor, suggesting that excess gut inflammation in CF is multi-factorial in aetiology. In this adult cohort, exocrine pancreatic function was irreversibly lost. Longer term follow-up may reveal more dynamic changes in the gut microbiota and possible restoration of CFTR function.


Asunto(s)
Fibrosis Quística , Microbiota , Adulto , Aminofenoles/farmacología , Regulador de Conductancia de Transmembrana de Fibrosis Quística/genética , Humanos , Inflamación , Lactoferrina/genética , Lactoferrina/farmacología , Complejo de Antígeno L1 de Leucocito , Mutación , Estudios Prospectivos , Quinolonas
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA