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Metabolism impacts upon Candida immunogenicity and pathogenicity at multiple levels.

Brown AJ, Brown GD, Netea MG, Gow NA - Trends Microbiol. (2014)

Bottom Line: Metabolism is integral to the pathogenicity of Candida albicans, a major fungal pathogen of humans.As well as providing the platform for nutrient assimilation and growth in diverse host niches, metabolic adaptation affects the susceptibility of C. albicans to host-imposed stresses and antifungal drugs, the expression of key virulence factors, and fungal vulnerability to innate immune defences.Therefore, current concepts of Candida-host interactions must be extended to include the impact of metabolic adaptation upon pathogenicity and immunogenicity.

View Article: PubMed Central - PubMed

Affiliation: Aberdeen Fungal Group, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK. Electronic address: al.brown@abdn.ac.uk.

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Changes in carbon source programme major changes in cell wall architecture. Transmission electron micrographs of the Candida albicans cell wall from cells grown on lactate or glucose as sole carbon source are shown on the left [33]. The cartoon on the right illustrates the structure of the C. albicans cell wall (adapted, with permission, from [76]).
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fig0005: Changes in carbon source programme major changes in cell wall architecture. Transmission electron micrographs of the Candida albicans cell wall from cells grown on lactate or glucose as sole carbon source are shown on the left [33]. The cartoon on the right illustrates the structure of the C. albicans cell wall (adapted, with permission, from [76]).

Mentions: Changes in carbon source exert dramatic effects on the C. albicans cell wall [33]. The cell wall has a characteristic architecture comprising a relatively thick inner lattice of β-glucan and chitin that is decorated with a dense coat of mannan fibrils (Figure 1) [6,44]. These mannans represent heavily N- and O-glycosylated proteins, many of which are covalently crosslinked to the carbohydrate infrastructure [45,46]. This structure has been defined for C. albicans cells grown on glucose. The relative proportions of β-glucan, chitin, and mannan are similar for glucose- and lactate-grown cells. However, cell wall biomass is significantly reduced after growth on lactate, and the cell walls of lactate-grown cells possess a β-glucan and chitin layer that is half the thickness of that for glucose-grown cells (Figure 1) [33]. The dynamics of these changes, which have not been described, probably depend upon the construction of new cell wall. Furthermore, significant changes were observed in the cell wall proteome [40]. Significantly, the levels of many cell wall remodelling enzymes were affected by carbon source, including glucanosyltransferases (Pga4, Phr1, and Phr2), glucosyltransferases (Bgl1), and transglycosylases (Crh11). Therefore, changes in crosslinking between cell wall biopolymers no doubt contribute to the altered biophysical properties of lactate-grown cell walls, which are more porous, more hydrophobic, and less elastic than those of glucose-grown cells [33].


Metabolism impacts upon Candida immunogenicity and pathogenicity at multiple levels.

Brown AJ, Brown GD, Netea MG, Gow NA - Trends Microbiol. (2014)

Changes in carbon source programme major changes in cell wall architecture. Transmission electron micrographs of the Candida albicans cell wall from cells grown on lactate or glucose as sole carbon source are shown on the left [33]. The cartoon on the right illustrates the structure of the C. albicans cell wall (adapted, with permission, from [76]).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4222764&req=5

fig0005: Changes in carbon source programme major changes in cell wall architecture. Transmission electron micrographs of the Candida albicans cell wall from cells grown on lactate or glucose as sole carbon source are shown on the left [33]. The cartoon on the right illustrates the structure of the C. albicans cell wall (adapted, with permission, from [76]).
Mentions: Changes in carbon source exert dramatic effects on the C. albicans cell wall [33]. The cell wall has a characteristic architecture comprising a relatively thick inner lattice of β-glucan and chitin that is decorated with a dense coat of mannan fibrils (Figure 1) [6,44]. These mannans represent heavily N- and O-glycosylated proteins, many of which are covalently crosslinked to the carbohydrate infrastructure [45,46]. This structure has been defined for C. albicans cells grown on glucose. The relative proportions of β-glucan, chitin, and mannan are similar for glucose- and lactate-grown cells. However, cell wall biomass is significantly reduced after growth on lactate, and the cell walls of lactate-grown cells possess a β-glucan and chitin layer that is half the thickness of that for glucose-grown cells (Figure 1) [33]. The dynamics of these changes, which have not been described, probably depend upon the construction of new cell wall. Furthermore, significant changes were observed in the cell wall proteome [40]. Significantly, the levels of many cell wall remodelling enzymes were affected by carbon source, including glucanosyltransferases (Pga4, Phr1, and Phr2), glucosyltransferases (Bgl1), and transglycosylases (Crh11). Therefore, changes in crosslinking between cell wall biopolymers no doubt contribute to the altered biophysical properties of lactate-grown cell walls, which are more porous, more hydrophobic, and less elastic than those of glucose-grown cells [33].

Bottom Line: Metabolism is integral to the pathogenicity of Candida albicans, a major fungal pathogen of humans.As well as providing the platform for nutrient assimilation and growth in diverse host niches, metabolic adaptation affects the susceptibility of C. albicans to host-imposed stresses and antifungal drugs, the expression of key virulence factors, and fungal vulnerability to innate immune defences.Therefore, current concepts of Candida-host interactions must be extended to include the impact of metabolic adaptation upon pathogenicity and immunogenicity.

View Article: PubMed Central - PubMed

Affiliation: Aberdeen Fungal Group, School of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK. Electronic address: al.brown@abdn.ac.uk.

Show MeSH
Related in: MedlinePlus