1 From Commensal to Pathogen: Candida albicans

Candida Survival Strategies

“…Alteration of the cell wall architecture will therefore ultimately lead to altered recognition responses, and indeed it has been shown that, for example, the growth of C. albicans on lactate stimulates the production of an anti-inflammatory IL-10 rather than proinflammatory IL-17 response by human peripheral blood mononuclear cells (PBMCs) (Ene, Cheng, Netea, & Brown, 2013). Metabolic adaptation is controlled by complex transcriptional networks in C. albicans, and a tight coregulation of metabolism and certain fitness or virulence attributes of C albicans during host colonization, commensalism, and pathogenicity has been described Brown, Odds, & Gow, 2007;Gow & Hube, 2012;Sabina & Brown, 2009;Whittington, Gow, & Hube, 2014). Thereby nutrient availability shapes the behavior of C. albicans and provides an environmental clue that might trigger invasion and infection.…”

Host-pathogen interactions between the human innate immune system and Candida albicans—understanding and modeling defense and evasion strategies

“…As a commensal C. albicans competes with all the probiotic microorganisms of the host's microflora for nutrients (Brunke and Hube, 2013 ; Whittington et al, 2014 ). Even though the gut is relatively rich in nutrients, those nutrients are quickly absorbed by the microbial flora and the epithelial cells (Whittington et al, 2014 ). In other host niches nutrients are limited by the host and usually not available to pathogens (see Table 1 ).…”

“…The diploid, polymorphic yeast Candida albicans (Wilson et al, 2009 ; Kwak et al, 2014 ; Mech et al, 2014 ) is one of the most important human pathogenic fungi (Lu et al, 2014 ; Vylkova and Lorenz, 2014 ; Whittington et al, 2014 ). This opportunistic ubiquitous fungus (Faro-Trindade and Brown, 2009 ; Zipfel et al, 2011 ; Bain et al, 2012 ) usually resides as a commensal on the skin and mucosal surfaces of 30 to 70 % of the human population (Cheng et al, 2012 ; Jacobsen et al, 2012 ; Quintin et al, 2014 ).…”

“…The homeostasis between C. albicans and the human host is kept by the human immune system (Luo et al, 2013 ; Yan et al, 2013 ; Vylkova and Lorenz, 2014 ) and the normal bacterial flora on mucosal surfaces and epithelial layers (Mayer et al, 2013 ; Yan et al, 2013 ; Mech et al, 2014 ). However, alterations in the host environment can render commensal factors into virulence attributes once the conditions favor pathogenicity (Moyes and Naglik, 2011 ; Bain et al, 2012 ; Whittington et al, 2014 ). Thus, there is a subtle balance between the commensal- and the pathogenic state of C. albicans .…”

Using Bayesian modelling to investigate factors governing antibiotic-induced Candida albicans colonization of the GI tract

“…The fungus Candida albicans is a human commensal that grows on the skin and mucosal surfaces of healthy individuals 1 . However, in susceptible patients, C. albicans can enter the bloodstream, either by translocation across the mucosa of the gastrointestinal (GI) tract 2 or via an indwelling vascular catheter 3 .…”