Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity

Simon Vautier, Rebecca A Drummond, Kong Chen, Graeme I Murray, David Kadosh, Alistair J P Brown, Neil A R Gow, Donna M MacCallum, Jay K Kolls, Gordon D Brown

Research output: Contribution to journalArticle

24 Citations (Scopus)
4 Downloads (Pure)

Abstract

The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.

Original languageEnglish
Pages (from-to)445-450
Number of pages6
JournalCellular Microbiology
Volume17
Issue number4
Early online date25 Nov 2014
DOIs
Publication statusPublished - Apr 2015

Fingerprint

Candida albicans
Gastrointestinal Tract
Immunity
Yeasts
Symbiosis
Anti-Bacterial Agents

Cite this

Candida albicans colonization and dissemination from the murine gastrointestinal tract : the influence of morphology and Th17 immunity. / Vautier, Simon; Drummond, Rebecca A; Chen, Kong; Murray, Graeme I; Kadosh, David; Brown, Alistair J P; Gow, Neil A R; MacCallum, Donna M; Kolls, Jay K; Brown, Gordon D.

In: Cellular Microbiology, Vol. 17, No. 4, 04.2015, p. 445-450.

Research output: Contribution to journalArticle

@article{c936678408324ce89968595bd9bd34fa,
title = "Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity",
abstract = "The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.",
author = "Simon Vautier and Drummond, {Rebecca A} and Kong Chen and Murray, {Graeme I} and David Kadosh and Brown, {Alistair J P} and Gow, {Neil A R} and MacCallum, {Donna M} and Kolls, {Jay K} and Brown, {Gordon D}",
note = "This article is protected by copyright. All rights reserved. This work was supported by the Wellcome Trust (086558, 080088, 102705), a Wellcome Trust Strategic Award (097377) and a studentship from the University of Aberdeen. D.K. was supported by grant 5R01AI083344 from the National Institute of Allergy and Infectious Diseases and by a Voelcker Young Investigator Award from the Max and Minnie Tomerlin Voelcker Fund.",
year = "2015",
month = "4",
doi = "10.1111/cmi.12388",
language = "English",
volume = "17",
pages = "445--450",
journal = "Cellular Microbiology",
issn = "1462-5814",
publisher = "Wiley-Blackwell",
number = "4",

}

TY - JOUR

T1 - Candida albicans colonization and dissemination from the murine gastrointestinal tract

T2 - the influence of morphology and Th17 immunity

AU - Vautier, Simon

AU - Drummond, Rebecca A

AU - Chen, Kong

AU - Murray, Graeme I

AU - Kadosh, David

AU - Brown, Alistair J P

AU - Gow, Neil A R

AU - MacCallum, Donna M

AU - Kolls, Jay K

AU - Brown, Gordon D

N1 - This article is protected by copyright. All rights reserved. This work was supported by the Wellcome Trust (086558, 080088, 102705), a Wellcome Trust Strategic Award (097377) and a studentship from the University of Aberdeen. D.K. was supported by grant 5R01AI083344 from the National Institute of Allergy and Infectious Diseases and by a Voelcker Young Investigator Award from the Max and Minnie Tomerlin Voelcker Fund.

PY - 2015/4

Y1 - 2015/4

N2 - The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.

AB - The ability of Candida albicans to cause disease is associated with its capacity to undergo morphological transition between yeast and filamentous forms, but the role of morphology in colonisation and dissemination from the gastrointestinal (GI) tract remains poorly defined. To explore this, we made use of wild type and morphological mutants of C. albicans in an established model of GI tract colonization, induced following antibiotic-treatment of mice. Our data reveal that GI tract colonization favours the yeast form of C. albicans, that there is constitutive low level systemic dissemination in colonized mice that occurs irrespective of fungal morphology, and that colonization is not controlled by Th17 immunity in otherwise immunocompetent animals. These data provide new insights into the mechanisms of pathogenesis and commensalism of C. albicans, and have implications for our understanding of human disease.

U2 - 10.1111/cmi.12388

DO - 10.1111/cmi.12388

M3 - Article

VL - 17

SP - 445

EP - 450

JO - Cellular Microbiology

JF - Cellular Microbiology

SN - 1462-5814

IS - 4

ER -