98%
921
2 minutes
20
While several environmental factors contribute to the evolutionary diversification of the pathogenic bacterium during cystic fibrosis lung infections, relatively little is known about the impact of the surrounding microbiota. By using experimental evolution we show that the presence of , or them both, prevent the evolution of loss of virulence, which repeatedly occurs in the absence of these species due to mutations in regulators of the Quinolone Signal quorum sensing system, and . Moreover, the strength of the effect of co-occurring species is attenuated through changes in the physical environment by the addition of mucin, resulting in selection for phenotypes resembling those evolved in the absence of the co-occurring species. Together, our findings show that variation in mucosal environment and the surrounding polymicrobial environment can determine the evolutionary trajectory of , partly explaining its diversification and pathoadaptation from acute to chronic phenotype during cystic fibrosis lung infections.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11067959 | PMC |
http://dx.doi.org/10.1093/ismeco/ycae043 | DOI Listing |
Front Microbiol
April 2025
Departamento de Microbiologia Médica, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Background: clonal complex 30 (CC30) is a historically significant pathogen affecting both hospital and community settings. The notable pandemic clones, phage-type 80/81 (PT80/81) and the Southwest Pacific clone (SWP) have spread internationally, contributing to significant morbidity and mortality. Despite their importance, research on the evolution of sequence type (ST) 30 has been limited, often focusing on a small number of strains or specific regions.
View Article and Find Full Text PDFISME Commun
January 2024
Department of Biology, University of York, Wentworth Way, York YO10 5DD, United Kingdom.
While several environmental factors contribute to the evolutionary diversification of the pathogenic bacterium during cystic fibrosis lung infections, relatively little is known about the impact of the surrounding microbiota. By using experimental evolution we show that the presence of , or them both, prevent the evolution of loss of virulence, which repeatedly occurs in the absence of these species due to mutations in regulators of the Quinolone Signal quorum sensing system, and . Moreover, the strength of the effect of co-occurring species is attenuated through changes in the physical environment by the addition of mucin, resulting in selection for phenotypes resembling those evolved in the absence of the co-occurring species.
View Article and Find Full Text PDFPLoS Pathog
June 2023
Department of Immunology and Microbiology, University of Colorado-Anschutz Medical Campus, School of Medicine, Aurora, Colorado, United States of America.
Insertion sequences (IS) are simple transposons implicated in the genome evolution of diverse pathogenic bacterial species. Enterococci have emerged as important human intestinal pathogens with newly adapted virulence potential and antibiotic resistance. These genetic features arose in tandem with large-scale genome evolution mediated by mobile elements.
View Article and Find Full Text PDFAdv Exp Med Biol
October 2022
Department of Clinical Microbiology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
Pseudomonas aeruginosa is an opportunistic pathogen that causes life-devastating acute as well as chronic biofilm-associated infections with limited treatment options. Its success is largely due to its remarkable adaptability. P.
View Article and Find Full Text PDFFront Cell Infect Microbiol
August 2022
Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, LA, United States.
Chronic respiratory infection (CRI) with (Pa) presents many unique challenges that complicate treatment. One notable challenge is the hypermutator phenotype which is present in up to 60% of sampled CRI patient isolates. Hypermutation can be caused by deactivating mutations in DNA mismatch repair (MMR) genes including , , and .
View Article and Find Full Text PDF