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

Research output: Contribution to journalArticlepeer-review

Standard

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 journalArticlepeer-review

Harvard

Vautier, S, Drummond, RA, Chen, K, Murray, GI, Kadosh, D, Brown, AJP, Gow, NAR, Maccallum, DM, Kolls, JK & Brown, GD 2015, 'Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity', Cellular Microbiology, vol. 17, no. 4, pp. 445-450. https://doi.org/10.1111/cmi.12388

APA

Vautier, S., Drummond, R. A., Chen, K., Murray, G. I., Kadosh, D., Brown, A. J. P., Gow, N. A. R., Maccallum, D. M., Kolls, J. K., & Brown, G. D. (2015). Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity. Cellular Microbiology, 17(4), 445-450. https://doi.org/10.1111/cmi.12388

Vancouver

Author

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. / Candida albicans colonization and dissemination from the murine gastrointestinal tract : the influence of morphology and Th17 immunity. In: Cellular Microbiology. 2015 ; Vol. 17, No. 4. pp. 445-450.

Bibtex

@article{4b97d6c5319844a58e39ff7170fb5102,
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 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.",
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.}",
year = "2015",
month = apr,
doi = "10.1111/cmi.12388",
language = "English",
volume = "17",
pages = "445--450",
journal = "Cellular Microbiology",
issn = "1462-5814",
publisher = "Wiley",
number = "4",

}

RIS

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.

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 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.

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 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.

UR - http://www.scopus.com/inward/record.url?scp=84924301501&partnerID=8YFLogxK

U2 - 10.1111/cmi.12388

DO - 10.1111/cmi.12388

M3 - Article

C2 - 25346172

AN - SCOPUS:84924301501

VL - 17

SP - 445

EP - 450

JO - Cellular Microbiology

JF - Cellular Microbiology

SN - 1462-5814

IS - 4

ER -