Fungal Factors Implicated in Pathogenesis

Cutler, Jim E.; Ye, Han

doi:10.1007/978-3-662-10373-9_1

Cited by 6 publications

(5 citation statements)

References 273 publications

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“…For example, C. dubliniensis appears to express higher levels of aspartyl proteases than C. albicans and to adhere as well as and possibly better than C. albicans to buccal epithelial cells (7,8,12,44). However, except for a few rare instances, the only host body site that is infected by C. dubliniensis is the oropharynx, while C. albicans can attack many body sites.…”

Section: Discussionmentioning

confidence: 99%

“…Examples of such characteristics include the inability to grow at 45°C, the production of multiple terminal chlamydoconidia, and assimilation of xylose. C. dubliniensis appears to have greater expression than C. albicans of some characteristics generally considered to be associated with virulence, such as aspartyl protease production and possibly adhesion to buccal epithelial cells (7,8,12,44), although its ability to bind to mucin appears similar to that of C. albicans (9). C. dubliniensis also appears to more easily develop resistance to fluconazole, which is commonly used to treat oropharyngeal candidiasis (6,56,57).…”

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confidence: 99%

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Comparison of the Hydrophobic Properties of Candida albicans and Candida dubliniensis

Hazen

Wu²,

Masuoka³

2001

Infect Immun

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Although Candida dubliniensis is a close genetic relative of Candida albicans, it colonizes and infects fewer sites. Nearly all instances of candidiasis caused by C. dubliniensis are restricted to the oral cavity. As cell surface hydrophobicity (CSH) influences virulence of C. albicans, CSH properties of C. dubliniensis were investigated and compared to C. albicans. Growth temperature is one factor which affects the CSH status of stationaryphase C. albicans. However, C. dubliniensis, similar to other pathogenic non-albicans species of Candida, was hydrophobic regardless of growth temperature. For all Candida species tested in this study (C. albicans, C. dubliniensis, C. glabrata, C. krusei, C. parapsilosis, and C. tropicalis), CSH status correlated with coaggregation with the anaerobic oral bacterium Fusobacterium nucleatum. Previous studies have shown that CSH status of C. albicans involves multiple surface proteins and surface protein N-glycans. The hydrophobic surface glycoprotein CAgp38 appears to be expressed by C. albicans constitutively regardless of growth temperature and medium. C. dubliniensis expresses a 38-kDa protein that cross-reacts with the anti-CAgp38 monoclonal antibody; however, expression of the protein was growth medium and growth temperature dependent. The anti-CAgp38 monoclonal antibody has been shown to inhibit adhesion of C. albicans to extracellular matrix proteins and to vascular endothelial cells. Since protein glycosylation influences the CSH status of C. albicans, we compared the cell wall mannoprotein content and composition between C. albicans and C. dubliniensis. Similar bulk compositional levels of hexose, phosphate, and protein in their N-glycans were determined. However, a component of the C. albicans N-glycan, acid-labile phosphooligomannoside, is expressed much less or negligibly by C. dubliniensis, and when present, the oligomannosides are predominantly less than five mannose residues in length. In addition, the acid-labile phosphooligomannoside profiles varied among the three strains of C. dubliniensis we tested, indicating the N-glycan of C. dubliniensis differs from C. albicans. For C. albicans, the acid-labile phosphooligomannoside influences virulence and surface fibrillar conformation, which affects exposure of hydrophobic surface proteins. Given the combined role in C. albicans of expression of specific surface hydrophobic proteins in pathogenesis and of surface protein glycosylation on exposure of the proteins, the lack of these virulence-associated CSH entities in C. dubliniensis could contribute to its limited ability to cause disseminated infections.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Comparison of the Hydrophobic Properties of Candida albicans and Candida dubliniensis

Hazen

Wu²,

Masuoka³

2001

Infect Immun

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“…While multiple host and fungal factors contribute to development of disseminated candidiasis (reviewed in references 39 and 44), the capacity of Candida albicans to adhere to many different host tissues is broadly considered a virulence trait to initiate invasive activity (12,29). The dissemination process likely begins by fungal cells gaining access to the bloodstream through gastrointestinal persorption, by seeding from a biofilm-fouled intramedic device, or through trauma-related inoculation (10,23,49).…”

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confidence: 99%

Inhibition of Hydrophobic Protein-MediatedCandida albicansAttachment to Endothelial Cells during Physiologic Shear Flow

Glee¹,

Cutler

Benson³

et al. 2001

Infect Immun

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“…Whereas enzymes secreted by melanized yeast cells and hyphae of Wangiella dermatitidis probably degrade human tissues in phaeohyphomycotic infections, the mechanical attributes of its cells also factor in virulence and disease progression (Brush and Money, 1999). Previous studies have identified the capacity for growth at 37°C as a minimum requirement for fungal pathogenicity against mammals (Cutler and Hahn, 1996). The ability to maintain invasive pressure at elevated temperatures may be a more critical qualification for a microorganism such as P. insidiosum whose hyphae penetrate solid tissues.…”

Section: Significance Of Hyphal Mechanics In Pathogenesismentioning

confidence: 98%