학술논문
A convergent evolutionary pathway attenuating cellulose production drives enhanced virulence of some bacteria.
Document Type
Academic Journal
Author
Nhu NTK; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia.; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Rahman MA; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Immunopathology Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.; QIMR Berghofer Medical Research Institute, Brisbane QLD, Australia.; Goh KGK; School of Pharmacy and Medical Sciences, Griffith University, Southport, QLD, Australia.; Menzies Health Institute Queensland, Griffith University, Southport, QLD, Australia.; Kim SJ; School of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.; Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia.; Phan MD; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia.; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Peters KM; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia.; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Alvarez-Fraga L; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; INRAE, Univ Montpellier, LBE, 102 Avenue des Etangs, Narbonne, 11100, France.; Hancock SJ; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK.; Ravi C; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia.; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Kidd TJ; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Central Microbiology, Pathology Queensland, Royal Brisbane and Women's Hospital, Brisbane, Australia.; Sullivan MJ; School of Pharmacy and Medical Sciences, Griffith University, Southport, QLD, Australia.; Menzies Health Institute Queensland, Griffith University, Southport, QLD, Australia.; School of Biological Sciences, University of East Anglia, Norwich, NR4 7TJ, UK.; Irvine KM; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Immunopathology Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia.; Beatson SA; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Sweet MJ; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; Irwin AD; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.; University of Queensland Centre for Clinical Research, Brisbane, Australia.; Queensland Children's Hospital, Brisbane, Australia.; Vukovic J; School of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia. j.vukovic@uq.edu.au.; Queensland Brain Institute, The University of Queensland, Brisbane, QLD, Australia. j.vukovic@uq.edu.au.; Ulett GC; School of Pharmacy and Medical Sciences, Griffith University, Southport, QLD, Australia. g.ulett@griffith.edu.au.; Menzies Health Institute Queensland, Griffith University, Southport, QLD, Australia. g.ulett@griffith.edu.au.; Hasnain SZ; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia. sumaira.hasnain@mater.uq.edu.au.; Immunopathology Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, Australia. sumaira.hasnain@mater.uq.edu.au.; Schembri MA; Institute for Molecular Bioscience (IMB), The University of Queensland, Brisbane, QLD, Australia. m.schembri@uq.edu.au.; School of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia. m.schembri@uq.edu.au.; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia. m.schembri@uq.edu.au.
Source
Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
Subject
Language
English
Abstract
Bacteria adapt to selective pressure in their immediate environment in multiple ways. One mechanism involves the acquisition of independent mutations that disable or modify a key pathway, providing a signature of adaptation via convergent evolution. Extra-intestinal pathogenic Escherichia coli (ExPEC) belonging to sequence type 95 (ST95) represent a global clone frequently associated with severe human infections including acute pyelonephritis, sepsis, and neonatal meningitis. Here, we analysed a publicly available dataset of 613 ST95 genomes and identified a series of loss-of-function mutations that disrupt cellulose production or its modification in 55.3% of strains. We show the inability to produce cellulose significantly enhances ST95 invasive infection in a rat model of neonatal meningitis, leading to the disruption of intestinal barrier integrity in newborn pups and enhanced dissemination to the liver, spleen and brain. Consistent with these observations, disruption of cellulose production in ST95 augmented innate immune signalling and tissue neutrophil infiltration in a mouse model of urinary tract infection. Mutations that disrupt cellulose production were also identified in other virulent ExPEC STs, Shigella and Salmonella, suggesting a correlative association with many Enterobacteriaceae that cause severe human infection. Together, our findings provide an explanation for the emergence of hypervirulent Enterobacteriaceae clones.
(© 2024. The Author(s).)
(© 2024. The Author(s).)