[1] Kennedy CB, Henington VM, Bordelon I, et al. Monilia (yeast-like) infections of the skin and mucous membrane[J].La State Med Soc,1954;106(11):419-423.
[2] Pappas PG, Kauffman CA, Andes D, et al. Clinical practice guidelines for the management of candidiasis:2009 update by the Infectious Diseases Society of America[J]. Clin Infect Dis, 2009,48(5):503-535.
[3] Sobel JD. Vulvovaginalcandidosis[J]. Lancet,2007,369(9577):1961-1971.
[4] Fidel PL, Jr. History and new insights into host defense against vaginal candidiasis[J]. Trends Microbiol,2004,12(5):220-227.
[5] Kathwate GH,Shinde RB and Karuppayil SM. Antiepileptic drugs inhibit growth,dimorphism,and biofilm mode of growth in human pathogen Candida albicans[J]. Assay Drug Dev Technol, 2015, 13(6):307-312.
[6] Matsubara VH,Wang Y,Bandara HM,et al. Probiotic lactobacilli inhibit early stages of Candida albicans biofilm development by reducing their growth,cell adhesion and filamentation[J]. Appl Microbiol Biotechnol,2016,100(14):64I5-6426.
[7] Perlroth J, Choi B, Spellberg B. Nosocomial fungal infections:epidemiology, diagnosis, and treatment[J].Med Mycol, 2007,45(4):321-346.
[8] Mayer FL,Wilson D,Hube B.Candida albicans pathogenicity mechanisms[J].Virulence,2013,4(2):119-128.
[9] Berman J, Sudbery PE. Candida albicans:a molecular revolution built on lessons from budding yeast[J]. Nat Rev Genet,2002,3(12):918-930.
[10] Brown GD, Denning DW, Levitz SM. Tackling human fungal infections[J]. Science,2012;336(6082):647.
[11] Sudbery P, Gow N, Berman J. The distinct morphogenic states of Candida albicans[J]. Trends Microbiol,2004,12(7):317-324.
[12] Sudbery PE. Growth of Candida albicans hyphae[J]. Nat Rev Microbiol,2011,9(10):737-748.
[13] Jacobsen ID, Wilson D, Wachtler B, et al. Candida albicans dimorphism as a therapeutic target[J]. Expert Rev Anti Infect Ther, 2012,10(1):85-93.
[14] Kumamoto CA. Molecular mechanisms of mechanosensing and their roles in fungal contact sensing[J]. Nat Rev Microbiol, 2008,6(9):667-673.
[15] Mitchell AP.Microbiology:Fungus produces a toxic surprise[J].Nature,2016,532(7597):41-42.
[16] Naglik JR, Moyes DL, Wachtler B, et al. Candida albicans interactions with epithelial cells and mucosal immunity[J]. Microbes Infect,2011,13(12-13):963-976.
[17] Dalle F, Wachtler B, L'Ollivier C, et al. Cellular interactions of Candida albicans with human oral epithelial cells and enterocytes[J]. Cell Microbiol,2010,12(2):248-271.
[18] Garcia MC, Lee JT, Ramsook CB, et al. A role for amyloid in cell aggregation and biofilm formation[J].PLoS One,2011,6(3):e17632.
[19] Murciano C, Moyes DL, Runglall M, et al. Evaluation of the role of Candida albicans agglutinin-like sequence (Als) proteins in human oral epithelial cell interactions[J]. PLoS One,2012,7(3):e33362.
[20] Lo HJ, Kohler JR, DiDomenico B, et al. Nonfilamentous C. albicans mutants are avirulent[J]. Cell,1997,90(5):939-949.
[21] Wachtler B, Wilson D, Haedicke K, et al. From attachment to damage:defined genes of Candida albicans mediate adhesion, invasion and damage during interaction with oral epithelial cells[J]. PLoS One,2011,6(2):e17046.
[22] 张辉,叶美花,余诚波,等.不同生物状态白念珠菌对口腔上皮细胞的黏附能力及ALSmRNA表达[J].中国医药导报,2015,26(12):16-19.
[23] 何淼,宋光泰,边专.白念珠菌ALS基因家族在生物膜形成过程中的差异表达[J].口腔医学研究,2015,31(10):957-960.
[24] Rast TJ,Kullas AL,Southern PJ,et al.Human epithelial cells ciscriminate between commensal and pathogenic interactions with Candida albicans[J]. PLoS One,2016,11(4):e0153165.cycle[J]. PLoSPathog,2010,6(3):e1000828.
[25] Wachtler B, Citiulo F, Jablonowski N, et al. Candida albicans-epithelial interactions:dissecting the roles of active penetration, induced endocytosis and host factors on the infection process[J]. PLoS One,2012,7(5):e36952.
[26] Wu H,Downs D,Ghosh K,et al.Candida albicans secreted aspartic proteases 4-6 induce apoptosis of epithelial cells by a novel Trojan horse mechanism[J].FASEB J, 2013, 27(6):2132-2144.
[27] Schaller M, Korting HC, Schafer W, et al. Secreted aspartic proteinase (Sap) activity contributes to tissue damage in a model of human oral candidosis[J]. Mol Microbiol,1999,34(1):169-180.
[28] Kumar R,Saraswat D,Tati S,et al.Novel aggregation properties of Candida albicans secreted aspartyl proteinase Sap6 mediate virulence in oral candidiasis[J].Infect Immun,2015,83(7):2614-2626.
[29] Niewerth M, Korting HC. Phospholipases of Candida albicans[J]. Mycoses, 2001,44(9-10):361-367.
[30] Theiss S, Ishdorj G, Brenot A, et al. Inactivation of the phospholipase B gene PLB5 in wild-type Candida albicans reduces cell-asso-ciated phospholipase A2 activity and attenuates virulence[J]. Int J Med Microbiol,2006,296(6):405-420.
[31] Gacser A, Stehr F, Kroger C, et al. Lipase 8 affects the pathogenesis of Candida albicans[J]. Infect Immun,2007,75(10):4710-4718.
[32] Sanders JW, Harless EL. Effects of practice on SISI scores and the relationship of SISI score to the intensity difference limen[J]. Am Audiol Soc,1976;2(3):95-98.
[33] Fanning S, Mitchell AP. Fungal biofilms[J]. PLos Pathogen, 2012,8(4):e1002585.
[34] Desai JV,Mitchell AP.Candida albicans biofilm development and its genetic control[J]. Microbiol Spectr,2015,3(3):10-16.
[35] Uppuluri P, Chaturvedi AK, Srinivasan A, et al. Dispersion as an important step in the Candida albicans biofilm developmental.
[36] Robbins N, Uppuluri P, Nett J, et al. Hsp90 governs dispersion and drug resistance of fungal biofilms[J]. PLos Pathogen. 2011,7(9):e1002257.
[37] Nobile CJ, Fox EP, Nett JE, et al. A recently evolved transcriptional network controls biofilm development in Candida albicans[J]. Cell, 2012,148(1-2):126-138.
[38] Caban M,Strapagiel D,Dziadek J,et al.Principles of a new protocol for prediction of azole resistance in Candida albicans infections on the basis of ERG11 polymorphisms[J].Curr Microbiol,2016,73(2):172-182.
[39] Brand A, Shanks S, Duncan VM, et al. Hyphal orientation of Candida albicans is regulated by a calcium-dependent mechanism[J]. Curr Biol,2007,17(4):347-352.
[40] Brand A, Gow NA. Mechanisms of hypha orientation of fungi[J]. Curr Opin Microbiol, 2009,12(4):350-357.