Genomic characterization of Pseudomonas aeruginosa adaptation mechanisms in bronchiectasis patients

Objectives Pseudomonas aeruginosa is one of the main causes of chronic bronchial infection (CBI), especially in patients with chronic underlying diseases such as cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD), asthma and bronchiectasis (BQ). Compared to P. aeruginosa CBI in CF, B...

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Detalles Bibliográficos
Autores: Muñoz Santa, Alba, Gómez Arbonés, Javier, Pifarré Teixidó, Ricardo, Garcia Gonzalez, Mercedes, Bellés Bellés, Alba
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2025
País:España
Institución:Universitat de Lleida (UdL)
Repositorio:Repositori Obert UdL
OAI Identifier:oai:repositori.udl.cat:10459.1/468737
Acceso en línea:https://doi.org/10.1515/almed-2025-0044
https://hdl.handle.net/10459.1/468737
Access Level:acceso abierto
Palabra clave:Bronchiectasis
Pseudomonas aeruginosa
Genomic adaptation
Descripción
Sumario:Objectives Pseudomonas aeruginosa is one of the main causes of chronic bronchial infection (CBI), especially in patients with chronic underlying diseases such as cystic fibrosis (CF), chronic obstructive pulmonary disease (COPD), asthma and bronchiectasis (BQ). Compared to P. aeruginosa CBI in CF, BQ infection has historically received less attention. The aim of this study was to determine the antibiotic susceptibility profile of 100 isolates recovered from 100 patients with P. aeruginosa CBI BQ and to characterize some of the adaptation mechanisms in 55 isolates by whole genome sequencing (WGS). Methods Susceptibility testing to 10 antipseudomonal agents was done by MicroScan WalkAway broth microdilution system. WGS was performed using the Illumina DNA Prep library preparation kit. Indexed libraries were sequenced on an Illumina MiSeq benchtop sequencer (300 base pairs paired-end reads). Results The most common loss-of-function mutations occurred in genes encoding the MexAB-OprM efflux-pump system, the pvd cluster and the fpvA receptor, and genes involved in twitching motility such as chpA and fimV. Conclusions Our data indicates that P. aeruginosa adapts by accumulating loss-of-function mutations in several genes, resulting in changes to different phenotypes that may guide the development of new alternative treatment therapies.