Pf Bacteriophage and Their Impact on Pseudomonas Virulence, Mammalian Immunity, and Chronic Infections

  • Patrick R. Secor
  • , Elizabeth B. Burgener
  • , M. Kinnersley
  • , Laura K. Jennings
  • , Valery Roman-Cruz
  • , Medeea Popescu
  • , Jonas D. Van Belleghem
  • , Naomi Haddock
  • , Conner Copeland
  • , Lia A. Michaels
  • , Christiaan R. de Vries
  • , Qingquan Chen
  • , Julie Pourtois
  • , Travis J. Wheeler
  • , Carlos E. Milla
  • , Paul L. Bollyky

Research output: Contribution to journalReview articlepeer-review

96 Scopus citations

Abstract

Pf bacteriophage are temperate phages that infect the bacterium Pseudomonas aeruginosa, a major cause of chronic lung infections in cystic fibrosis (CF) and other settings. Pf and other temperate phages have evolved complex, mutualistic relationships with their bacterial hosts that impact both bacterial phenotypes and chronic infection. We and others have reported that Pf phages are a virulence factor that promote the pathogenesis of P. aeruginosa infections in animal models and are associated with worse skin and lung infections in humans. Here we review the biology of Pf phage and what is known about its contributions to pathogenesis and clinical disease. First, we review the structure, genetics, and epidemiology of Pf phage. Next, we address the diverse and surprising ways that Pf phages contribute to P. aeruginosa phenotypes including effects on biofilm formation, antibiotic resistance, and motility. Then, we cover data indicating that Pf phages suppress mammalian immunity at sites of bacterial infection. Finally, we discuss recent literature implicating Pf in chronic P. aeruginosa infections in CF and other settings. Together, these reports suggest that Pf bacteriophage have direct effects on P. aeruginosa infections and that temperate phages are an exciting frontier in microbiology, immunology, and human health.

Original languageEnglish
Article number244
JournalFrontiers in Immunology
Volume11
DOIs
StatePublished - Feb 21 2020

Funding

Funding. PS was supported by NIH grants R01AI138981 and K22AI125282. PS and TW were supported by NIH grant P20GM103546. JV and CV were supported by grant T32 AI007502-22. PB was supported by grants R21AI133370, R21AI133240, R01AI12492093, grants from Stanford SPARK, the Falk Medical Research Trust, and the Cystic Fibrosis Foundation (CFF). MP was supported by a NSFGRF grant. EB was supported by grant T32 HL129970 and the Stanford Maternal Child Health Research Institute. CM was supported by grant R01 HL148184 and Ross Mosier CF Laboratories Research Fund.

Funder number
T32 HL129970
T32 AI007502-22, P20GM103546, R01AI12492093, K22AI125282, R01AI138981, R21AI133240
R21AI133370
R01 HL148184

    Keywords

    • Inovirus
    • Pf phage
    • Pseudomonas aeruginosa
    • bacteriophage
    • cystic fibrosis
    • immunology
    • infection
    • wound

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