Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth

Abstract Candida spp. adhere to medical devices, such as catheters, forming drug-tolerant biofilms that resist killing by the immune system. Little is known about how C. glabrata, an emerging pathogen, resists attack by phagocytes. Here we show that upon encounter with planktonic (non-biofilm) C. gl...

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Autores principales:	Chad J. Johnson, John F. Kernien, Amanda R. Hoyer, Jeniel E. Nett
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/01124bf4f9b7437db972c6c60c83bc6f
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spelling	oai:doaj.org-article:01124bf4f9b7437db972c6c60c83bc6f2021-12-02T15:05:19ZMechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth10.1038/s41598-017-13588-62045-2322https://doaj.org/article/01124bf4f9b7437db972c6c60c83bc6f2017-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-13588-6https://doaj.org/toc/2045-2322Abstract Candida spp. adhere to medical devices, such as catheters, forming drug-tolerant biofilms that resist killing by the immune system. Little is known about how C. glabrata, an emerging pathogen, resists attack by phagocytes. Here we show that upon encounter with planktonic (non-biofilm) C. glabrata, human neutrophils initially phagocytose the yeast and subsequently release neutrophil extracellular traps (NETs), complexes of DNA, histones, and proteins capable of inhibiting fungal growth and dissemination. When exposed to C. glabrata biofilms, neutrophils also release NETs, but significantly fewer than in response to planktonic cells. Impaired killing of biofilm parallels the decrease in NET production. Compared to biofilm, neutrophils generate higher levels of reactive oxygen species (ROS) when presented with planktonic organisms, and pharmacologic inhibition of NADPH-oxidase partially impairs NET production. In contrast, inhibition of phagocytosis nearly completely blocks NET release to both biofilm and planktonic organisms. Imaging of the host response to C. glabrata in a rat vascular model of infection supports a role for NET release in vivo. Taken together, these findings show that C. glabrata triggers NET release. The diminished NET response to C. glabrata biofilms likely contributes to the resilience of these structured communities to host defenses.Chad J. JohnsonJohn F. KernienAmanda R. HoyerJeniel E. NettNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Chad J. Johnson John F. Kernien Amanda R. Hoyer Jeniel E. Nett Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
description	Abstract Candida spp. adhere to medical devices, such as catheters, forming drug-tolerant biofilms that resist killing by the immune system. Little is known about how C. glabrata, an emerging pathogen, resists attack by phagocytes. Here we show that upon encounter with planktonic (non-biofilm) C. glabrata, human neutrophils initially phagocytose the yeast and subsequently release neutrophil extracellular traps (NETs), complexes of DNA, histones, and proteins capable of inhibiting fungal growth and dissemination. When exposed to C. glabrata biofilms, neutrophils also release NETs, but significantly fewer than in response to planktonic cells. Impaired killing of biofilm parallels the decrease in NET production. Compared to biofilm, neutrophils generate higher levels of reactive oxygen species (ROS) when presented with planktonic organisms, and pharmacologic inhibition of NADPH-oxidase partially impairs NET production. In contrast, inhibition of phagocytosis nearly completely blocks NET release to both biofilm and planktonic organisms. Imaging of the host response to C. glabrata in a rat vascular model of infection supports a role for NET release in vivo. Taken together, these findings show that C. glabrata triggers NET release. The diminished NET response to C. glabrata biofilms likely contributes to the resilience of these structured communities to host defenses.
format	article
author	Chad J. Johnson John F. Kernien Amanda R. Hoyer Jeniel E. Nett
author_facet	Chad J. Johnson John F. Kernien Amanda R. Hoyer Jeniel E. Nett
author_sort	Chad J. Johnson
title	Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
title_short	Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
title_full	Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
title_fullStr	Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
title_full_unstemmed	Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth
title_sort	mechanisms involved in the triggering of neutrophil extracellular traps (nets) by candida glabrata during planktonic and biofilm growth
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/01124bf4f9b7437db972c6c60c83bc6f
work_keys_str_mv	AT chadjjohnson mechanismsinvolvedinthetriggeringofneutrophilextracellulartrapsnetsbycandidaglabrataduringplanktonicandbiofilmgrowth AT johnfkernien mechanismsinvolvedinthetriggeringofneutrophilextracellulartrapsnetsbycandidaglabrataduringplanktonicandbiofilmgrowth AT amandarhoyer mechanismsinvolvedinthetriggeringofneutrophilextracellulartrapsnetsbycandidaglabrataduringplanktonicandbiofilmgrowth AT jenielenett mechanismsinvolvedinthetriggeringofneutrophilextracellulartrapsnetsbycandidaglabrataduringplanktonicandbiofilmgrowth
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Mechanisms involved in the triggering of neutrophil extracellular traps (NETs) by Candida glabrata during planktonic and biofilm growth

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