Pyoverdine, a siderophore from Pseudomonas aeruginosa, translocates into C. elegans, removes iron, and activates a distinct host response

Donghoon Kang, Daniel R. Kirienkoa, Phillip Webster, Alfred L. Fisher, Natalia V. Kirienko

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

Pseudomonas aeruginosa, a re-emerging, opportunistic human pathogen, encodes a variety of virulence determinants. Pyoverdine, a siderophore produced by this bacterium, is essential for pathogenesis in mammalian infections. This observation is generally attributed to its roles in acquiring iron and/or regulating other virulence factors. Here we report that pyoverdine translocates into the host, where it binds and extracts iron. Pyoverdine-mediated iron extraction damages host mitochondria, disrupting their function and triggering mitochondrial turnover via autophagy. The host detects this damage via a conserved mitochondrial surveillance pathway mediated by the ESRE network. Our findings illuminate the pathogenic mechanisms of pyoverdine and highlight the importance of this bacterial product in host-pathogen interactions.

Original languageEnglish (US)
Pages (from-to)804-817
Number of pages14
JournalVirulence
Volume9
Issue number1
DOIs
StatePublished - Jan 1 2018

Keywords

  • Caenorhabditis elegans
  • Host response
  • Mitochondrial damage
  • Pathogenesis
  • Pseudomonas aeruginosa
  • Pyoverdine
  • Siderophore

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Microbiology (medical)
  • Infectious Diseases

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