Candida albicans colonization and dissemination from the murine gastrointestinal tract: the influence of morphology and Th17 immunity. (25th November 2014)

• Record Type: Journal Article
• Authors: 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.
• Is Part Of: Cellular microbiology. Volume 17:Number 4(2015:Apr.)
• Page Start: 445
• Page End: 450
• Publication Date: 2014-11-25
• Subjects: Microbiology -- Periodicals; Cytology -- Periodicals; Host-parasite relationships -- Periodicals; Microbiology -- Periodicals; Cells -- Periodicals; Microbiologie -- Périodiques; Microbiologie; Relation hôte-parasite; Cytologie; Cellule; Réponse cellulaire; Ressource Internet (Descripteur de forme); Périodique électronique (Descripteur de forme); 579.05
• DOI: 10.1111/cmi.12388
• Languages: English
• ISSNs: 1462-5814

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>The ability of <italic>C</italic><italic>andida albicans</italic> 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 <italic>C</italic><italic>. albicans</italic> 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 <italic>C</italic><italic>. albicans</italic>, 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 <italic>C</italic><italic>. albicans</italic>, and have implications for our understanding of human disease.</p> </abstract>