Epithelial discrimination of commensal and pathogenic Candida albicans

被引:29
作者
Tang, S. X. [1 ]
Moyes, D. L. [1 ]
Richardson, J. P. [1 ]
Blagojevic, M. [1 ]
Naglik, J. R. [1 ]
机构
[1] Kings Coll London, Inst Dent, Mucosal & Salivary Biol Div, London SE1 1UL, England
基金
英国生物技术与生命科学研究理事会;
关键词
Candida albicans; epithelium; innate; immunity; MAPK; c-Fos; VULVO-VAGINAL CANDIDIASIS; TH17; CELLS; OROPHARYNGEAL CANDIDIASIS; ANTIFUNGAL DEFENSE; HOST RESPONSE; GENE FAMILY; INFECTION; IMMUNITY; RECOGNITION; MECHANISMS;
D O I
10.1111/odi.12395
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
All mucosal surfaces are lined by epithelial cells and are colonised by opportunistic microbes. In health, these opportunistic microbes remain commensal and are tolerated by the immune system. However, when the correct environmental conditions arise, these microbes can become pathogenic and need to be controlled or cleared by the immune system to prevent disease. The mechanisms that enable epithelial cells to initiate the danger' signals activated specifically by pathogenic microbes are critical to mucosal defence and homeostasis but are not well understood. Deciphering these mechanisms will provide essential understanding to how mucosal tissues maintain health and activate immunity, as well as how pathogens promote disease. This review focuses on the interaction of the human fungal pathogen Candida albicans with epithelial cells and the epithelial mechanisms that enable mucosal tissues to discriminate between the commensal and pathogenic state of this medically important fungus.
引用
收藏
页码:114 / 119
页数:6
相关论文
共 49 条
[41]   Candida albicans-Epithelial Interactions: Dissecting the Roles of Active Penetration, Induced Endocytosis and Host Factors on the Infection Process [J].
Waechtler, Betty ;
Citiulo, Francesco ;
Jablonowski, Nadja ;
Foerster, Stephanie ;
Dalle, Frederic ;
Schaller, Martin ;
Wilson, Duncan ;
Hube, Bernhard .
PLOS ONE, 2012, 7 (05)
[42]   From Attachment to Damage: Defined Genes of Candida albicans Mediate Adhesion, Invasion and Damage during Interaction with Oral Epithelial Cells [J].
Waechtler, Betty ;
Wilson, Duncan ;
Haedicke, Katja ;
Dalle, Frederic ;
Hube, Bernhard .
PLOS ONE, 2011, 6 (02)
[43]   Regulation of innate immune response by MAP kinase phosphatase-1 [J].
Wang, Xianxi ;
Liu, Yusen .
CELLULAR SIGNALLING, 2007, 19 (07) :1372-1382
[44]   Epithelial Cells and Innate Antifungal Defense [J].
Weindl, G. ;
Wagener, J. ;
Schaller, M. .
JOURNAL OF DENTAL RESEARCH, 2010, 89 (07) :666-675
[45]   Human epithelial cells establish direct antifungal defense through TLR4-mediated signaling [J].
Weindl, Guenther ;
Naglik, Julian R. ;
Kaesler, Susanne ;
Biedermann, Tilo ;
Hube, Bernhard ;
Korting, Hans Christian ;
Schaller, Martin .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (12) :3664-3672
[46]   Cytokines in the host response to Candida vaginitis: Identifying a role for non-classical immune mediators, S100 alarmins [J].
Yano, Junko ;
Noverr, Mairi C. ;
Fidel, Paul L., Jr. .
CYTOKINE, 2012, 58 (01) :118-128
[47]   In vivo transcript profiling of Candida albicans identifies a gene essential for interepithelial dissemination [J].
Zakikhany, Katherina ;
Naglik, Julian R. ;
Schmidt-Westhausen, Andrea ;
Holland, Gudrun ;
Schaller, Martin ;
Hube, Bernhard .
CELLULAR MICROBIOLOGY, 2007, 9 (12) :2938-2954
[48]   EGFR and HER2 receptor kinase signaling mediate epithelial cell invasion by Candida albicans during oropharyngeal infection [J].
Zhu, Weidong ;
Phan, Quynh T. ;
Boontheung, Pinmanee ;
Solis, Norma V. ;
Loo, Joseph A. ;
Filler, Scott G. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2012, 109 (35) :14194-14199
[49]   Interactions of Candida albicans with epithelial cells [J].
Zhu, Weidong ;
Filler, Scott G. .
CELLULAR MICROBIOLOGY, 2010, 12 (03) :273-282