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Candida albicans escapes from mouse neutrophils

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  • David Ermert
  • Maria J Niemiec
  • Marc Röhm
  • Andreas Glenthøj
  • Niels Borregaard
  • Constantin F Urban
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Candida albicans, the most commonly isolated human fungal pathogen, is able to grow as budding yeasts or filamentous forms, such as hyphae. The ability to switch morphology has been attributed a crucial role for the pathogenesis of C. albicans. To mimic disseminated candidiasis in humans, the mouse is the most widely used model organism. Neutrophils are essential immune cells to prevent opportunistic mycoses. To explore potential differences between the rodent infection model and the human host, we compared the interactions of C. albicans with neutrophil granulocytes from mice and humans. We revealed that murine neutrophils exhibited a significantly lower ability to kill C. albicans than their human counterparts. Strikingly, C. albicans yeast cells formed germ tubes upon internalization by murine neutrophils, eventually rupturing the neutrophil membrane and thereby, killing the phagocyte. On the contrary, growth and subsequent escape of C. albicans are blocked inside human neutrophils. According to our findings, this blockage in human neutrophils might be a result of higher levels of MPO activity and the presence of α-defensins. We therefore outline differences in antifungal immune defense between humans and mouse strains, which facilitates a more accurate interpretation of in vivo results.
Original languageEnglish
JournalJournal of Leukocyte Biology
Volume94
Issue number2
Pages (from-to)223-36
Number of pages14
ISSN0741-5400
DOIs
Publication statusPublished - Aug 2013

    Research areas

  • Animals, Candida albicans, Female, Gene Knock-In Techniques, Humans, Hyphae, Immune Evasion, Immunity, Innate, Male, Mice, Mice, Inbred C57BL, Models, Animal, Neutrophils, Peroxidase, Reactive Oxygen Species, Recombinant Fusion Proteins, Respiratory Burst, Species Specificity, alpha-Defensins

ID: 42570860