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      Host carbon sources modulate cell wall architecture, drug resistance and virulence in a fungal pathogen

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          Abstract

          The survival of all microbes depends upon their ability to respond to environmental challenges. To establish infection, pathogens such as Candida albicans must mount effective stress responses to counter host defences while adapting to dynamic changes in nutrient status within host niches. Studies of C. albicans stress adaptation have generally been performed on glucose-grown cells, leaving the effects of alternative carbon sources upon stress resistance largely unexplored. We have shown that growth on alternative carbon sources, such as lactate, strongly influence the resistance of C. albicans to antifungal drugs, osmotic and cell wall stresses. Similar trends were observed in clinical isolates and other pathogenic Candida species. The increased stress resistance of C. albicans was not dependent on key stress (Hog1) and cell integrity (Mkc1) signalling pathways. Instead, increased stress resistance was promoted by major changes in the architecture and biophysical properties of the cell wall. Glucose- and lactate-grown cells displayed significant differences in cell wall mass, ultrastructure, elasticity and adhesion. Changes in carbon source also altered the virulence of C. albicans in models of systemic candidiasis and vaginitis, confirming the importance of alternative carbon sources within host niches during C. albicans infections.

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          Most cited references70

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          Epidemiology of invasive mycoses in North America.

          The incidence of invasive mycoses is increasing, especially among patients who are immunocompromised or hospitalized with serious underlying diseases. Such infections may be broken into two broad categories: opportunistic and endemic. The most important agents of the opportunistic mycoses are Candida spp., Cryptococcus neoformans, Pneumocystis jirovecii, and Aspergillus spp. (although the list of potential pathogens is ever expanding); while the most commonly encountered endemic mycoses are due to Histoplasma capsulatum, Coccidioides immitis/posadasii, and Blastomyces dermatitidis. This review discusses the epidemiologic profiles of these invasive mycoses in North America, as well as risk factors for infection, and the pathogens' antifungal susceptibility.
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            Immune sensing of Candida albicans requires cooperative recognition of mannans and glucans by lectin and Toll-like receptors.

            The fungal pathogen Candida albicans has a multilayered cell wall composed of an outer layer of proteins glycosylated with N- or O-linked mannosyl residues and an inner skeletal layer of beta-glucans and chitin. We demonstrate that cytokine production by human mononuclear cells or murine macrophages was markedly reduced when stimulated by C. albicans mutants defective in mannosylation. Recognition of mannosyl residues was mediated by mannose receptor binding to N-linked mannosyl residues and by TLR4 binding to O-linked mannosyl residues. Residual cytokine production was mediated by recognition of beta-glucan by the dectin-1/TLR2 receptor complex. C. albicans mutants with a cell wall defective in mannosyl residues were less virulent in experimental disseminated candidiasis and elicited reduced cytokine production in vivo. We concluded that recognition of C. albicans by monocytes/macrophages is mediated by 3 recognition systems of differing importance, each of which senses specific layers of the C. albicans cell wall.
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              Atomic force microscope.

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                Author and article information

                Journal
                Cell Microbiol
                Cell. Microbiol
                cmi
                Cellular Microbiology
                Blackwell Publishing Ltd
                1462-5814
                1462-5822
                September 2012
                05 June 2012
                : 14
                : 9
                : 1319-1335
                Affiliations
                [1 ]Aberdeen Fungal Group, School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen Foresterhill, Aberdeen, AB25 2ZD, UK
                [2 ]Division of Biotechnology and Forensic Sciences, School of Contemporary Sciences, University of Abertay Dundee Dundee, DD1 1HG, UK
                Author notes
                *For correspondence. E-mail al.brown@ 123456abdn.ac.uk ; Tel. (+44) 1224 437482; Fax (+44) 1224 437465.

                Re-use of this article is permitted in accordance with the Terms and Conditions set out at http://wileyonlinelibrary.com/onlineopen#OnlineOpen_Terms.

                Article
                10.1111/j.1462-5822.2012.01813.x
                3465787
                22587014
                13e21eff-fbca-4503-bce7-eeaf17974663
                Copyright © 2012 Blackwell Publishing Ltd

                Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

                History
                : 07 March 2012
                : 19 April 2012
                : 09 May 2012
                Categories
                Editors' Choice

                Microbiology & Virology
                Microbiology & Virology

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