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 journalArticlepeer-review

    63 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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