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.Peer reviewedPublisher PD

Brown, Alistair J P

Brown, Gordon D

Chen, Kong

Drummond, Rebecca A

Gow, Neil A R

Kadosh, David

Kolls, Jay K

MacCallum, Donna M

Murray, Graeme I

Vautier, Simon

Cellular Microbiology

English

PubMed

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 colonization 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. Candida albicans is a commensal of the human gastrointestinal (GI) tract but can also spread from this site to cause systemic disease following immune perturbation. Here, using morphologically-locked strains we show that although the yeast form is favoured in the GI tract, both the yeast and hyphal forms can disseminate from this site to distal tissues in healthy animals. Finally, we show that Th17 immunity has no role in fungal colonisation or dissemination from the GI tract.</p

Drummond, Rebecca A.

Murray, Graeme I.

Brown, Alistair J.P.

Gow, Neil A.R.

Maccallum, Donna M.

Kolls, Jay K.

Brown, Gordon D.

University of Birmingham Research Portal

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

Crossref

<i>C</i><i>andida albicans</i>colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity

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.Peer reviewe

Aberdeen University Research

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

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

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University of Birmingham Research Portal

Aberdeen University Research