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Open AccessJournal ArticleDOI

Neutrophil extracellular traps capture and kill Candida albicans yeast and hyphal forms

TLDR
It is shown for the first time that Candida albicans, a eukaryotic pathogen, induces NET‐formation and is susceptible to NET‐mediated killing, and that granule components mediate fungal killing.
Abstract
Neutrophils phagocytose and kill microbes upon phagolysosomal fusion. Recently we found that activated neutrophils form extracellular fibres that consist of granule proteins and chromatin. These neutrophil extracellular traps (NETs) degrade virulence factors and kill Gram positive and negative bacteria. Here we show for the first time that Candida albicans, a eukaryotic pathogen, induces NET-formation and is susceptible to NET-mediated killing. C. albicans is the predominant aetiologic agent of fungal infections in humans, particularly in immunocompromised hosts. One major virulence trait of C. albicans is its ability to reversibly switch from singular budding cells to filamentous hyphae. We demonstrate that NETs kill both yeast-form and hyphal cells, and that granule components mediate fungal killing. Taken together our data indicate that neutrophils trap and kill ascomycetous yeasts by forming NETs.

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Citations
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Novel cell death program leads to neutrophil extracellular traps

TL;DR: This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan.
Journal ArticleDOI

Surface phenotype and antigenic specificity of human interleukin 17–producing T helper memory cells

TL;DR: It is demonstrated that human TH-17 cells have distinct migratory capacity and antigenic specificities and a link between microbial products, T helper cell differentiation and homing in response to fungal antigens is established.
Journal ArticleDOI

Neutrophil extracellular traps in immunity and disease

TL;DR: The identification of molecules that modulate the release of NETs has helped to refine the view of the role of neutrophils in immune protection, inflammatory and autoimmune diseases and cancer.
Journal ArticleDOI

Neutrophil elastase and myeloperoxidase regulate the formation of neutrophil extracellular traps

TL;DR: Neutrophil elastase escapes azurophilic granules, translocates to the nucleus, and degrades histones to promote chromatin decondensation necessary for NET formation.
Journal ArticleDOI

Neutrophil Extracellular Traps Contain Calprotectin, a Cytosolic Protein Complex Involved in Host Defense against Candida albicans

TL;DR: The present investigations confirmed the antifungal activity of calprotectin in vitro and demonstrated that it contributes to effective host defense against C. albicans in vivo.
References
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Journal ArticleDOI

Innate Immune Recognition

TL;DR: Microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens to distinguish infectious nonself from noninfectious self.
Journal ArticleDOI

Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
Journal ArticleDOI

How neutrophils kill microbes

TL;DR: Killing was previously believed to be accomplished by oxygen free radicals and other reactive oxygen species generated by the NADPH oxidase, and by oxidized halides produced by myeloperoxidase, but this is incorrect.
Journal ArticleDOI

Inside the neutrophil phagosome: oxidants, myeloperoxidase, and bacterial killing.

TL;DR: Neutrophils are one of the professional phagocytes in humans that ingest bacteria into intracellular spaces and are involved in phagocytosis.
Journal ArticleDOI

Immunity to fungal infections

TL;DR: Research in this field is entering an exciting period of transition from studying the molecular and cellular bases of fungal virulence to determining the cellular and molecular mechanisms that maintain immune homeostasis with fungi.
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