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Evolution and host-specific adaptation of Pseudomonas aeruginosa.
Weimann, Aaron; Dinan, Adam M; Ruis, Christopher; Bernut, Audrey; Pont, Stéphane; Brown, Karen; Ryan, Judy; Santos, Lúcia; 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.
Afiliación
  • Weimann A; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Dinan AM; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Ruis C; Cambridge Centre for AI in Medicine, University of Cambridge, Cambridge, UK.
  • Bernut A; Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.
  • Pont S; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Brown K; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Ryan J; Cambridge Centre for AI in Medicine, University of Cambridge, Cambridge, UK.
  • Santos L; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Ellison L; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Ukor E; Cambridge Centre for AI in Medicine, University of Cambridge, Cambridge, UK.
  • Pandurangan AP; Department of Veterinary Medicine, University of Cambridge, Cambridge, UK.
  • Krokowski S; Laboratory of Pathogens and Host Immunity (LPHI), UMR5235, CNRS/Université de Montpellier, Montpellier, France.
  • Blundell TL; Laboratory of Pathogens and Host Immunity (LPHI), UMR5235, CNRS/Université de Montpellier, Montpellier, France.
  • Welch M; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Blane B; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Judge K; Cambridge Centre for Lung Infection, Royal Papworth Hospital, Cambridge, UK.
  • Bousfield R; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Brown N; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Bryant JM; Department of Physiology, Bioscience Institute, University College Cork, Cork, Ireland.
  • Kukavica-Ibrulj I; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Rampioni G; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Leoni L; Cambridge Centre for Lung Infection, Royal Papworth Hospital, Cambridge, UK.
  • Harrison PT; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Peacock SJ; Department of Biochemistry, University of Cambridge, Cambridge, UK.
  • Thomson NR; Department of Medicine, University of Cambridge, Cambridge, UK.
  • Gauthier J; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Fothergill JL; University of Cambridge Molecular Immunity Unit, MRC Laboratory of Molecular Biology, Cambridge, UK.
  • Levesque RC; Victor Phillip Dahdaleh Heart & Lung Research Institute, University of Cambridge, Cambridge, UK.
  • Parkhill J; Department of Biochemistry, University of Cambridge, Cambridge, UK.
  • Floto RA; Department of Medicine, University of Cambridge, Cambridge, UK.
Science ; 385(6704): eadi0908, 2024 Jul 05.
Article en En | MEDLINE | ID: mdl-38963857
ABSTRACT
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.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Fibrosis Quística Límite: Humans Idioma: En Revista: Science Año: 2024 Tipo del documento: Article País de afiliación: Reino Unido

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Pseudomonas aeruginosa / Infecciones por Pseudomonas / Fibrosis Quística Límite: Humans Idioma: En Revista: Science Año: 2024 Tipo del documento: Article País de afiliación: Reino Unido