Host-pathogen interactions and virulence-associated genes during Candida albicans oral infections

被引:52
|
作者
Martin, Ronny [1 ,2 ,4 ]
Waechtler, Betty [1 ]
Schaller, Martin [3 ]
Wilson, Duncan [1 ]
Hube, Bernhard [1 ,4 ]
机构
[1] HKI, Leibniz Inst Nat Prod Res & Infect Biol, Dept Microbial Pathogen Mechanisms, D-07745 Jena, Germany
[2] HKI, Leibniz Inst Nat Prod Res & Infect Biol, Ctr Innovat Competence Sept, Res Grp Fungal Sept, D-07745 Jena, Germany
[3] Univ Tubingen, Dept Dermatol, Tubingen, Germany
[4] Univ Jena, Jena, Germany
关键词
C; albicans; Oral infections; Transcriptional profiling; Virulence-associated genes; N-TERMINAL DOMAIN; RECONSTITUTED HUMAN EPITHELIA; BIOFILM FORMATION; IN-VITRO; OROPHARYNGEAL CANDIDIASIS; PSEUDOMONAS-AERUGINOSA; VAGINAL CANDIDIASIS; IMPROVES SURVIVAL; EXPRESSION; MODEL;
D O I
10.1016/j.ijmm.2011.04.009
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Oral infections with Candida albicans are very common diseases in even only mildly immunocompromised patients. By using genome-wide microarrays, in vitro infection models and samples from patients with pseudomembranous candidiasis, several genes have been identified which encode known and unknown fungal factors associated with oral infection. The expression of selected genes has been investigated via qRT-PCR in both in vitro models and in vivo samples from patients. Several lines of evidence suggest that fungal morphology plays a key role in adhesion to and invasion into oral epithelial cells and mutants lacking regulators of hyphal formation are attenuated in their ability to invade and damage epithelial cells. Adhesion is mediated by hyphal-associated factors such as Hwp1 and the Als adhesin family. Hyphal formation facilitates epithelial invasion via two routes: active penetration and induced endocytosis. While induced endocytosis is predominantly mediated by the adhesin and invasin Als3, active penetration seems to be supported by hydrolase activity and mechanical pressure. Expression profiles reflect the morphological switch and an adaptive response to neutral pH, non-glucose carbon sources, and nitrosative stress. (C) 2011 Elsevier GmbH. All rights reserved.
引用
收藏
页码:417 / 422
页数:6
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