Evolution and host-specific adaptation of Pseudomonas aeruginosa

成果类型:
Article
署名作者:
Weimann, Aaron; Dinan, Adam M.; Ruis, Christopher; Bernut, Audrey; Pont, Stephane; Brown, Karen; Ryan, Judy; Santos, Lucia; Ellison, Louise; Ukor, Emem; Pandurangan, Arun P.; Krokowski, Sina; Blundell, Tom L.; Welch, Martin; Blane, Beth; Judge, Kim; Bousfield, Rachel; Brown, Nicholas; Bryant, Josephine M.; Kukavica-Ibrulj, Irena; Rampioni, Giordano; Leoni, Livia; Harrison, Patrick T.; Peacock, Sharon J.; Thomson, Nicholas R.; Gauthier, Jeff; Fothergill, Jo L.; Levesque, Roger C.; Parkhill, Julian; Floto, R. Andres
署名单位:
University of Cambridge; MRC Laboratory Molecular Biology; University of Cambridge; University of Cambridge; University of Cambridge; Centre National de la Recherche Scientifique (CNRS); Universite de Montpellier; Papworth Hospital; University College Cork; University of Cambridge; University of Cambridge; Wellcome Trust Sanger Institute; Laval University; Italfarmaco; Roma Tre University; IRCCS Santa Lucia; University of London; London School of Hygiene & Tropical Medicine; University of Liverpool
刊物名称:
SCIENCE
ISSN/ISSBN:
0036-11818
DOI:
10.1126/science.adi0908
发表日期:
2024-07-05
关键词:
cystic-fibrosis air-pollution genome DISCOVERY infection Visualization annotation expression FRAMEWORK CHILDREN
摘要:
The major human bacterial pathogen Pseudomonas aeruginosa causes multidrug-resistant infections in people with underlying immunodeficiencies or structural lung diseases such as cystic fibrosis (CF). We show that a few environmental isolates, driven by horizontal gene acquisition, have become dominant epidemic clones that have sequentially emerged and spread through global transmission networks over the past 200 years. These clones demonstrate varying intrinsic propensities for infecting CF or non-CF individuals (linked to specific transcriptional changes enabling survival within macrophages); have undergone multiple rounds of convergent, host-specific adaptation; and have eventually lost their ability to transmit between different patient groups. Our findings thus explain the pathogenic evolution of P. aeruginosa and highlight the importance of global surveillance and cross-infection prevention in averting the emergence of future epidemic clones.