Research on molecular mechanisms of Candida albicans infection

Abstract

Abstract:

Candida albicans is the most common human opportunistic fungal pathogen which have to cope with mechanical(e.g., epithelial) barriers, biochemical, chemical, and physical antagonists(e.g., bile, mucus, pH), and the innate and adaptive immune system of thehost during its invading.Candida albicans's biochemistry, morphology flexibility and the ability to escape the host innate immunity plays crucial pathogenic roles.In this review we present an update on current understanding of the molecular mechanisms of infection of this pathogen in order to provide the reference to further explore new drugs.

Key words: Candida albicans, infection, molecular mechanisms

CLC Number:

R379.4

KANG Ye, ZHOU Mi, Yan Lan. Research on molecular mechanisms of Candida albicans infection[J]. Chinese Journal of Mycology, 2015, 10(5): 312-316.

References

[1] Peleg AY,Hogan DA,Mylonakis E.Medically important bacterial-fungal interactions[J].Nat Rev Microbiol,2010,8(5):340-349.
[2] 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.
[3] Pfaller MA,Diekema DJ.Epidemiology of invasive mycoses in North America[J].Crit Rev Microbiol,2010,36(1):1-53.
[4] Gow NA,van de Veerdonk FL,Brown AJ.Netea MG.Candida albicans morphogenesis and host defence:discriminating invasion from colonization[J].Nat Rev Microbiol,2012,10(2):112-122.
[5] Inglis DO,Sherlock G.Ras signaling gets fine-tuned:regulation of multiple pathogenic traits of Candida albicans[J].Eukaryot Cell,2013,12(10):1316-1325.
[6] Shareck J,Belhumeur P.Modulation of morphogenesis in Candida albicans by various small molecules[J].Eukaryot Cell.2011,10(8):1004-1012.
[7] Sudbery PE.Growth of Candida albicans hyphae[J].Nat Rev Microbiol,2011,9(10):737-748.
[8] Lu Y,Su C,Solis NV,Filler SG,et al.Synergistic regulation of hyphal elongation by hypoxia,CO(2),and nutrient conditions controls the virulence of Candida albicans[J].Cell Host & Microbe,2013,14(5):499-509.
[9] Su C,Lu Y,Liu H.Reduced TOR signaling sustains hyphal development in Candida albicans by lowering Hog1 basal activity[J].Mol Biol Cell,2013,24(3):385-397.
[10] Pierce JV,Dignard D,Whiteway M,et al.Normal adaptation of Candida albicans to the murine gastrointestinal tract requires Efg1p-dependent regulation of metabolic and host defense genes[J].Eukaryot Cell,2013,12(1):37-49.
[11] Lee IR,Morrow CA,Fraser JA.Nitrogen regulation of virulence in clinically prevalent fungal pathogens[J].FEMS Microbiol Lett,2013,345(2):77-84.
[12] Navarathna DH,Das A,Morschhauser J,et al.Dur3 is the major urea transporter in Candida albicans and is co-regulated with the urea amidolyase Dur1,2[J].Microbiology,2011,57(Pt 1):270-279.
[13] Vylkova S,Carman AJ,Danhof HA,et al.The fungal pathogen Candida albicans autoinduces hyphal morphogenesis by raising extracellular pH[J].MBio,2011,2(3):e00055-11.
[14] Lorenz MC,Bender JA,Fink GR.Transcriptional response of Candida albicans upon internalization by macrophages[J].Eukaryot Cell,2004,3(5):1076-1087.
[15] Ghosh S,Navarathna DH,Roberts DD,et al.Arginine-induced germ tube formation in Candida albicans is essential for escape from murine macrophage line RAW 264.7[J].Infect Immu,2009,77(4):1596-1605.
[16] Xu H,Nobile CJ,Dongari-Bagtzoglou A.Glucanase induces filamentation of the fungal pathogen Candida albicans[J].PLoS One,2013,8(5):e63736.
[17] 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.
[18] 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.
[19] 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.
[20] 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.
[21] Sundstrom P,Cutler JE,Staab JF.Reevaluation of the role of HWP1 in systemic candidiasis by use of Candida albicans strains with selectable marker URA3 targeted to the ENO1 locus[J].Infect Immu,2002,70(6):3281-3283.
[22] Nobile CJ,Schneider HA,Nett JE,et al.Complementary adhesin function in C.albicans biofilm formation[J].Curr Biol,2008,18(14):1017-1024.
[23] Zhu W,Filler SG.Interactions of Candida albicans with epithelial cells[J].Cell Microbiol.2010;12(3):273-82.
[24] Sandini S,La Valle R,De Bernardis F,et al.The 65 kDa mannoprotein gene of Candida albicans encodes a putative beta-glucanase adhesin required for hyphal morphogenesis and experimental pathogenicity[J].Cell Microbiol,2007,9(5):1223-1238.
[25] De Bernardis F,Liu H,O'Mahony R,et al.Human domain antibodies against virulence traits of Candida albicans inhibit fungus adherence to vaginal epithelium and protect against experimental vaginal candidiasis[J].J Infect Dis,2007,195(1):149-157.
[26] 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.
[27] Park H,Myers CL,Sheppard DC,et al.Role of the fungal Ras-protein kinase A pathway in governing epithelial cell interactions during oropharyngeal candidiasis[J].Cell Microbiol,2005,7(4):499-510.
[28] Villar CC,Zhao XR.Candida albicans induces early apoptosis followed by secondary necrosis in oral epithelial cells[J].Mol Oral Microbiol,2010,25(3):215-225.
[29] Phan QT,Myers CL,Fu Y,et al.Als3 is a Candida albicans invasin that binds to cadherins and induces endocytosis by host cells[J].PLoS Biol,2007,5(3):e64.
[30] Phan QT,Fratti RA,Prasadarao NV,et al.Filler SG.N-cadherin mediates endocytosis of Candida albicans by endothelial cells[J].J Biol Chem,2005,280(11):10455-10461.
[31] Sun JN,Solis NV,Phan QT,et al.Host cell invasion and virulence mediated by Candida albicans Ssa1[J].PLoS Pathog,2010,6(11):e1001181.
[32] 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.
[33] Naglik JR,Challacombe SJ,Hube B.Candida albicans secreted aspartyl proteinases in virulence and pathogenesis[J].Microbiol Mol Biol Rev,2003,67(3):400-428,table of contents.
[34] Zakikhany K,Naglik JR,Schmidt-Westhausen A,et al.In vivo transcript profiling of Candida albicans identifies a gene essential for interepithelial dissemination[J].Cell Microbiol,2007,9(12):2938-2954.
[35] Villar CC,Kashleva H,Nobile CJ,et al.Mucosal tissue invasion by Candida albicans is associated with E-cadherin degradation,mediated by transcription factor Rim101p and protease Sap5p[J].Infect Immu,2007,75(5):2126-2135.
[36] Borelli C,Ruge E,Lee JH,et al.X-ray structures of Sap1 and Sap5:structural comparison of the secreted aspartic proteinases from Candida albicans[J].Proteins,2008,72(4):1308-1319.
[37] Gropp K,Schild L,Schindler S,et al.The yeast Candida albicans evades human complement attack by secretion of aspartic proteases[J].Mol Immunol,2009,47(2-3):465-475.
[38] Niewerth M,Korting HC.Phospholipases of Candida albicans[J].Mycoses,2001,44(9-10):361-367.
[39] Yang P,Du H,Hoffman CS,et al.The phospholipase B homolog Plb1 is a mediator of osmotic stress response and of nutrient-dependent repression of sexual differentiation in the fission yeast Schizosaccharomyces pombe[J].Mol Genet Genomics,2003;269(1):116-125.
[40] Köohler GA,Brenot A,Haas-Stapleton E,et al.Phospholipase A2 and phospholipase B activities in fungi[J].Biochim Biophys Acta,2006,1761(11):1391-1399.
[41] Paraje MG,Correa SG,Albesa I,et al.Lipase of Candida albicans induces activation of NADPH oxidase and L-arginine pathways on resting and activated macrophages[J].Biochem Biophys Res Commun,2009,390(2):263-268.
[42] Gacser A,Stehr F,Kroger C,et al.Lipase 8 affects the pathogenesis of Candida albicans[J].Infect Immun,2007,75(10):4710-4718.
[43] Fanning S,Mitchell AP.Fungal biofilms[J].PLoS Pathog,2012,8(4):e1002585.
[44] Finkel JS,Mitchell AP.Genetic control of Candida albicans biofilm development[J].Nat Rev Microbiol,2011,9(2):109-118.
[45] Uppuluri P,Chaturvedi AK,Srinivasan A,et al.Dispersion as an important step in the Candida albicans biofilm developmental cycle[J].PLoS Pathog,2010,6(3):e1000828.
[46] Robbins N,Uppuluri P,Nett J,et al.Hsp90 governs dispersion and drug resistance of fungal biofilms[J].PLoS Pathog,2011,7(9):e1002257.
[47] 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.
[48] Nobile CJ,Nett JE,Hernday AD,et al.Biofilm matrix regulation by Candida albicans Zap1[J].PLoS Biol,2009,7(6):e1000133.
[49] Taff HT,Nett JE,Zarnowski R,et al,Sanchez H,Cain MT,et al.A Candida biofilm-induced pathway for matrix glucan delivery:implications for drug resistance[J].PLoS Pathog,2012,8(8):e1002848.
[50] Xie Z,Thompson A,Sobue T,et al.Candida albicans biofilms do not trigger reactive oxygen species and evade neutrophil killing[J].J Infect Dis,2012,206(12):1936-1945.
[51] Missall TA,Lodge JK,McEwen JE.Mechanisms of resistance to oxidative and nitrosative stress:implications for fungal survival in mammalian hosts[J].Eukaryot Cell,2004,3(4):835-846.
[52] Lopes da Rosa J,Boyartchuk VL,Zhu LJ,et al.Histone acetyltransferase Rtt109 is required for Candida albicans pathogenesis[J].Proc Natl Acad Sci USA,2010,107(4):1594-1599.
[53] Frohner IE,Bourgeois C,Yatsyk K,et al.Candida albicans cell surface superoxide dismutases degrade host-derived reactive oxygen species to escape innate immune surveillance[J].Mol Microbiol,2009,71(1):240-252.
[54] Shi QM,Wang YM,Zheng XD,et al.Critical role of DNA checkpoints in mediating genotoxic-stress-induced filamentous growth in Candida albicans[J].Mol Biol Cell,2007,18(3):815-826.