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Cellular Microbiology: Pathogen-Host Cell Molecular Interactions

Candida albicans Ras1 Inactivation Increases Resistance to Phagosomal Killing by Human Neutrophils

Ornella Salvatori, Ruvini U. Pathirana, Jason G. Kay, Mira Edgerton
George S. Deepe, Editor
Ornella Salvatori
aDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, New York, USA
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Ruvini U. Pathirana
aDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, New York, USA
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Jason G. Kay
aDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, New York, USA
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Mira Edgerton
aDepartment of Oral Biology, School of Dental Medicine, University at Buffalo, Buffalo, New York, USA
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George S. Deepe
University of Cincinnati
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DOI: 10.1128/IAI.00685-18
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ABSTRACT

Host phagocytic cells are crucial players in initial defense against Candida albicans infection. C. albicans utilizes MAP kinases and Ras1 stress response signaling pathways to protect itself from killing by immune cells. In this study, we tested the importance of these pathways in C. albicans phagocytosis by neutrophils and subsequent phagosomal survival. Phagocytosis was influenced by C. albicans morphology, so hyphal length of >10 μm reduced the phagocytic index (PI) 2- to 3-fold in human neutrophils. Primary human neutrophils killed 81% of phagocytosed C. albicans, while primary mouse neutrophils killed 63% of yeasts. We found that both the C. albicans Cek1 and Hog1 pathways were required for survival of phagocytosed yeast, whereas deletion of C. albicans RAS1 resulted in an 84% increase in survival within neutrophils compared to that of the wild type (WT). The absence of Ras1 did not alter reactive oxygen species (ROS) production by C. albicans; however, phagocytosed C. albicans Δ/Δras1 cells reduced ROS release by neutrophils by 86%. Moreover, C. albicans Δ/Δras1 cells had increased resistance to hydrogen peroxide as a result of high levels of catalase activity. This phenotype was specific to Ras1, since these effects were not observed in the absence of its partner Cyr1 or with its downstream target Efg1. In addition, C. albicans Δ/Δras1 cells had a significantly increased resistance to nonoxidative killing by human neutrophil peptide 1 (HNP-1) that was reversed by restoring cellular cAMP levels. These data show that C. albicans Ras1 inactivation leads to fungal resistance to both oxidative and nonoxidative mechanisms of neutrophil phagosomal killing.

FOOTNOTES

    • Received 6 September 2018.
    • Accepted 20 September 2018.
    • Accepted manuscript posted online 24 September 2018.
  • Supplemental material for this article may be found at https://doi.org/10.1128/IAI.00685-18.

  • Copyright © 2018 American Society for Microbiology.

All Rights Reserved.

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Candida albicans Ras1 Inactivation Increases Resistance to Phagosomal Killing by Human Neutrophils
Ornella Salvatori, Ruvini U. Pathirana, Jason G. Kay, Mira Edgerton
Infection and Immunity Nov 2018, 86 (12) e00685-18; DOI: 10.1128/IAI.00685-18

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Candida albicans Ras1 Inactivation Increases Resistance to Phagosomal Killing by Human Neutrophils
Ornella Salvatori, Ruvini U. Pathirana, Jason G. Kay, Mira Edgerton
Infection and Immunity Nov 2018, 86 (12) e00685-18; DOI: 10.1128/IAI.00685-18
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KEYWORDS

Candida albicans
human neutrophils
phagocytosis
Ras1

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