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Relationship between Candida albicans Virulence during Experimental Hematogenously Disseminated Infection and Endothelial Cell Damage In Vitro
Open accessAbstract
Candida albicans must penetrate the endothelial cell lining of the vasculature to invade the deep tissues during a hematogenously disseminated infection. We compared 27 C. albicans mutants with their wild-type parent for their capacity to damage endothelial cells in vitro and cause a lethal infection in mice following tail vein inoculation. Of 10 mutants with significantly impaired capacity to damage endothelial cells, all had attenuated virulence. Therefore, the endothelial cell damage assay can be used as a screen to identify some virulence factors relevant to hematogenously disseminated candidiasis.
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“We have found previously that C. albicans mutants with defects in the signal transduction pathways that govern hyphal formation have a significantly reduced capacity to invade both endothelial and oral epithelial cells in vitro [5][6][7].”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [6]
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“Host cell invasion and damage are likely critical virulence attributes of C. albicans because mutants with defects in these processes in vitro are highly likely to have attenuated virulence in experimental animal models of hematogenously disseminated or oropharyngeal candidiasis [5][6][7][8].”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [6]
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Cites
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Self-citation
Cited by
Sorted by citations
Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells
Phan, Q. T., Myers, C. L., Fu, Y., Sheppard, D. C., Yeaman, M. R., Welch, W. H., Ibrahim, A. S., Edwards, J. E., & Filler, S. G. (2007) · PLoS Biology · doi:10.1371/journal.pbio.0050064 · Cited by 641
Self-citationGenetic control of Candida albicans biofilm development
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Self-citationCritical Role of Bcr1-Dependent Adhesins in C. albicans Biofilm Formation In Vitro and In Vivo
Nobile, C. J., Andes, D. R., Nett, J. E., Smith, F. J., Yue, F., Phan, Q.-T., Edwards, J. E., Filler, S. G., & Mitchell, A. P. (2006) · PLoS Pathogens · doi:10.1371/journal.ppat.0020063 · Cited by 507
“CAI4-URA3 ura3D::kimm434 ARG4::pARG4-URA3 [38]”
BackgroundSelf-citationRegulation of Cell-Surface Genes and Biofilm Formation by the C. albicans Transcription Factor Bcr1p
Nobile, C. J., & Mitchell, A. P. (2005) · Current Biology · doi:10.1016/j.cub.2005.05.047 · Cited by 464
Self-citationLin, L., Ibrahim, A. S., Xu, X., Farber, J. M., Avanesian, V., Baquir, B., Fu, Y., French, S. W., Edwards, J. E., & Spellberg, B. J. (2009) · PLoS Pathogens · doi:10.1371/journal.ppat.1000703 · Cited by 474
“albicans [6,50,51], as evidenced by the superior efficacy seen in the current study with another clinical bloodstream isolate of C.”
BackgroundSelf-citationDispersion as an Important Step in the Candida albicans Biofilm Developmental Cycle
Uppuluri, P., Chaturvedi, A. K., Srinivasan, A., Banerjee, M., Ramasubramaniam, A. K., Köhler, J. R., Kadosh, D., & Lopez-Ribot, J. L. (2010) · PLoS Pathogens · doi:10.1371/journal.ppat.1000828 · Cited by 432
“albicans biofilms display enhanced adhesion to endothelial cells and cause increased endothelial cell damage Establishment of metastatic foci of infection of Candida species, a critical step in the pathogenesis of deep organ candidiasis, is presumably dependent on the fungus traversing the vascular endothelium [41,42].”
BackgroundFunction of Candida albicans Adhesin Hwp1 in Biofilm Formation
Nobile, C. J., Nett, J. E., Andes, D. R., & Mitchell, A. P. (2006) · Eukaryotic Cell · doi:10.1128/ec.00194-06 · Cited by 395
“HWP1) (20), CAI4-URA3 (reference strain) (15), CAYF178U (als3/als3)”
Self-citationCandida albicans Als3, a multifunctional adhesin and invasin
Liu, Y., & Filler, S. G. (2011) · Eukaryotic Cell · doi:10.1128/ec.00279-10 · Cited by 354
“albicans mutants with impaired capacity to invade and damage host cells in vitro frequently have attenuated virulence in murine models of oropharyngeal and hematogenously disseminated candidiasis (12, 39, 43, 51, 61).”
BackgroundSelf-citationHost Cell Invasion and Virulence Mediated by Candida albicans Ssa1
Sun, J. N., Solis, N. V., Phan, Q. T., Bajwa, J. S., Kashleva, H., Thompson, A., Liu, Y., Dongari-Bagtzoglou, A., Edgerton, M., & Filler, S. G. (2010) · PLoS Pathogens · doi:10.1371/journal.ppat.1001181 · Cited by 220
“The virulence of the various strains was tested in the mouse model of hematogenously disseminated candidiasis as described previously [26].”
BackgroundSelf-citationPark, H., Myers, C. L., Sheppard, D. C., Phan, Q. T., Sanchez, A. A., E. Edwards, J., & Filler, S. G. (2004) · Cellular Microbiology · doi:10.1111/j.1462-5822.2004.00476.x · Cited by 207
“Fu (Sanchez et al., 2004) HLC67 efg1D::hisG/efg1D::hisG G.”
MethodInfluentialSelf-citationThewes, S., Kretschmar, M., Park, H., Schaller, M., Filler, S. G., & Hube, B. (2007) · Molecular Microbiology · doi:10.1111/j.1365-2958.2007.05614.x · Cited by 140
“To induce haematogenously disseminated candidiasis, male Balb/C mice were infected via the lateral tail vein with 5 ¥ 105 blastospores of C. albicans as previously described (Sanchez et al., 2004).”
MethodSelf-citationAspergillus fumigatusMedA governs adherence, host cell interactions and virulence
Gravelat, F. N., Ejzykowicz, D. E., Chiang, L. Y., Chabot, J. C., Urb, M., MacDonald, K., Al-Bader, N., Filler, S. G., & Sheppard, D. C. (2009) · Cellular Microbiology · doi:10.1111/j.1462-5822.2009.01408.x · Cited by 138
“…sexual development often directly regulate the expression of key virulence factors (Lo et al., 1997; Lengeler et al., 2000; Phan et al., 2000; Sonneborn et al., 2000; Bahn and Sundstrom, 2001, Felk et al., 2002; Fu et al., 2002; Garcia-Sanchez et al., 2004; Sanchez et al., 2004; Park et al., 2005).”
BackgroundSelf-citationDijck, P. V., Sjollema, J., Cammue, B. P. A., Lagrou, K., Berman, J. G., d’Enfert, C., Andes, D. R., Arendrup, M. C., Brakhage, A. A., Calderone, R., et al. (2018) · Microbial Cell · doi:10.15698/mic2018.07.638 · Cited by 136
“as well as other fungal pathogens [292-294].”
Self-citationRequirement for Candida albicans Sun41 in Biofilm Formation and Virulence
Norice, C. T., Smith, F. J., Solis, N. V., Filler, S. G., & Mitchell, A. P. (2007) · Eukaryotic Cell · doi:10.1128/ec.00314-07 · Cited by 122
“Second, the sun41 /sun41 mutant had no defect in endothelial cell damage, while all other hypha-defective mutants tested have such a defect (41).”
BackgroundSelf-citationCandida albicansand cancer: Can this yeast induce cancer development or progression?
Ramirez‐Garcia, A., Rementería, A., Urízar, J. M. A., Moragues, M. D., Antoran, A., Pellón, A., Abad, A., & Hernando, F. L. (2014) · Critical Reviews in Microbiology · doi:10.3109/1040841x.2014.913004 · Cited by 128
“…et al., 1995, 1996; Glee et al., 2001; Grubb et al., 2009; Jong et al., 2003; Kurihara et al., 2003; Lim et al., 2011; Mayer et al., 2012; Orozco et al., 2000; Park et al., 2009; Phan et al., 2000;Ramirez-Garcia et al., 2011, 2013; Sanchez et al., 2004; Seidl et al., 2012; Zhao et al., 2007).”
BackgroundSherwani, M. A., Tufail, S., Khan, A. A., & Owais, M. (2015) · PLoS ONE · doi:10.1371/journal.pone.0131684 · Cited by 114
“Besides assisting host defence evasion, hyphal transformants are lethal to macrophages and endothelial cells [35, 36].”
BackgroundSwidergall, M., Khalaji, M., Solis, N. V., Moyes, D. L., Drummond, R. A., Hube, B., Lionakis, M. S., Murdoch, C., Filler, S. G., & Naglik, J. R. (2019) · The Journal of Infectious Diseases · doi:10.1093/infdis/jiz322 · Cited by 119
“Virulence of the C albicans strains was tested in the mouse model of HDC using 6- to 7-week-old male and female BALB/c mice (Taconics) as previously described [35].”
MethodSelf-citationDivergent Targets of Candida albicans Biofilm Regulator Bcr1 In Vitro and In Vivo
Fanning, S., Xu, W., Solis, N., Woolford, C. A., Filler, S. G., & Mitchell, A. P. (2012) · Eukaryotic Cell · doi:10.1128/ec.00103-12 · Cited by 106
Self-citationActivation and Alliance of Regulatory Pathways in C. albicans during Mammalian Infection
Xu, W., Solis, N. V., Ehrlich, R. L., Woolford, C. A., Filler, S. G., & Mitchell, A. P. (2015) · PLOS Biology · doi:10.1371/journal.pbio.1002076 · Cited by 103
“albicans were inoculated intravenously with 5 × 10(5) yeastphase cells that had been grown in YPD at 30°C to saturation as described previously [46].”
MethodSelf-citationMayer, F. L., Wilson, D., Jacobsen, I. D., Miramón, P., Slesiona, S., Bohovych, I., Brown, A. J. P., & Hube, B. (2012) · PLoS ONE · doi:10.1371/journal.pone.0038584 · Cited by 101
“[22,108,109,110].”
Mechanisms of Candida albicans Trafficking to the Brain
Liu, Y., Mittal, R., Solis, N. V., Prasadarao, N. V., & Filler, S. G. (2011) · PLoS Pathogens · doi:10.1371/journal.ppat.1002305 · Cited by 93
“albicans strains [50] and then monitored for survival three times daily.”
BackgroundSelf-citationInvasive Phenotype ofCandida albicansAffects the Host Proinflammatory Response to Infection
Villar, C. C., Kashleva, H., Mitchell, A. P., & Dongari‐Bagtzoglou, A. I. (2005) · Infection and Immunity · doi:10.1128/iai.73.8.4588-4595.2005 · Cited by 89
“albicans to host cells (32, 44); therefore, downregulation of these proteins in the rim101 /rim101 mutant might contribute to its reduced ability to invade and damage host cells and tissues, as demonstrated in this study and by other workers (11, 42).”
BackgroundResultSelf-citationRouabhia, M., Schaller, M., Corbucci, C., Vecchiarelli, A., Prill, S. K. ‐., Giasson, L., & Ernst, J. F. (2005) · Infection and Immunity · doi:10.1128/iai.73.8.4571-4580.2005 · Cited by 90
“Reduced virulence of the pmt1 mutant was expected because of its significant defect in hyphal morphogenesis, its leakage of cell wall proteins, including chitinase, its supersensitivity to antifungal agents directed against wall components, its lack of adhesion to Caco-2 cells, and its lower virulence in an HDC model…”
BackgroundResultGrubb, S. E. W., Murdoch, C., Sudbery, P. E., Saville, S. P., Lopez-Ribot, J. L., & Thornhill, M. H. (2008) · Infection and Immunity · doi:10.1128/iai.00332-08 · Cited by 87
“albicans is necessary for the organism to damage endothelial cells (22, 67) and that substances that inhibit germination block C.”
BackgroundLü, Y., Su, C., Solis, N. V., Filler, S. G., & Liu, H. (2013) · Cell Host & Microbe · doi:10.1016/j.chom.2013.10.008 · Cited by 87
“The virulence of the various strains was analyzed in the mouse model of hematogenously disseminated candidiasis as described previously (Sanchez et al., 2004; Sun et al., 2010).”
BackgroundSelf-citationNew signaling pathways govern the host response to C. albicans infection in various nichesPreprint
Liu, Y., Shetty, A. C., Schwartz, J. A. J., Bradford, L. L., Xu, W., Phan, Q. T., Kumari, P., Mahurkar, A., Mitchell, A. P., Ravel, J., et al. (2015) · Genome Research · doi:10.5281/zenodo.13524844 · Cited by 88
“The observation that invasion-defective C. albicans mutants display attenuated virulence in murine models of OPC and HDC is evidence of the critical importance of invasion to virulence (Phan et al. 2000; Sanchez et al. 2004; Park et al. 2005; Chiang et al. 2007).”
BackgroundSelf-citationMartínez-López, R., Park, H., Myers, C., Gil, C., & Filler, S. (2006) · Eukaryotic Cell · doi:10.1128/ec.5.1.140-147.2006 · Cited by 81
“albicans that are endocytosed poorly and cause little damage to endothelial cells and oral epithelial cells have significantly reduced virulence in mouse models of hematogenously disseminated or oropharyngeal candidiasis (20, 21, 25).”
BackgroundSelf-citationGlucose Sensing Network in Candida albicans : a Sweet Spot for Fungal Morphogenesis
Sabina, J., & Brown, V. E. (2009) · Eukaryotic Cell · doi:10.1128/ec.00138-09 · Cited by 85
“vitro (90), and efg1 null mutants show reduced virulence during blood infections (78).”
Iron metabolism in aerobes: Managing ferric iron hydrolysis and ferrous iron autoxidation
Kosman, D. J. (2012) · Coordination Chemistry Reviews · doi:10.1016/j.ccr.2012.06.030 · Cited by 82
Mai, H., Champion, L., Ouali, N., Hertig, A., Péraldi, M., Glotz, D., Rondeau, É., Costa, M.-A., Snanoudj, R., Benoît, G., et al. (2006) · Transplantation · doi:10.1097/01.tp.0000239188.27153.23 · Cited by 74
“The reasons why some cases of Candida contamination led to mycotic arteritis while others did not are not clear, although the difference in Candida virulence that determines its capacity to penetrate endothelial cells may be one of the explanations (13).”
BackgroundBrand, A., Vacharaksa, A., Bendel, C. M., Norton, J., Haynes, P. R., Henry‐Stanley, M. J., Wells, C. L., Ross, K., Gow, N. A. R., & Gale, C. A. (2008) · Eukaryotic Cell · doi:10.1128/ec.00453-07 · Cited by 73
“albicans strains reported to have reduced cytotoxicity are unable to form hyphae (41, 51, 53).”
BackgroundToenjes, K. A., Munsee, S. M., Ibrahim, A. S., Jeffrey, R., Edwards, J. E., & Johnson, D. I. (2005) · Antimicrobial Agents and Chemotherapy · doi:10.1128/aac.49.3.963-972.2005 · Cited by 72
“albicans virulence during experimental hematogenously disseminated infection and endothelial cell damage in vitro (35).”
BackgroundMatignon, M., Botterel, F., Audard, V., Dunogué, B., Dahan, K., Lang, P., Bretagne, S., & Grimbert, P. (2008) · American Journal of Transplantation · doi:10.1111/j.1600-6143.2007.02112.x · Cited by 70
“glabrata, tropicalis or krusei have been reported (17,18).”
BackgroundAdhesion of Candida albicans to Endothelial Cells under Physiological Conditions of Flow
Grubb, S. E. W., Murdoch, C., Sudbery, P. E., Saville, S. P., Lopez-Ribot, J. L., & Thornhill, M. H. (2009) · Infection and Immunity · doi:10.1128/iai.00518-09 · Cited by 66
The Novel Candida albicans Transporter Dur31 Is a Multi-Stage Pathogenicity Factor
Mayer, F. L., Wilson, D., Jacobsen, I. D., Miramón, P., Große, K., & Hube, B. (2012) · PLoS Pathogens · doi:10.1371/journal.ppat.1002592 · Cited by 62
“albicans mutants with reduced capacity to damage endothelial cells in vitro, often display reduced virulence in mice models of hematogenously disseminated candidiasis [56].”
BackgroundTranscriptional Responses of Candida albicans to Epithelial and Endothelial Cells
Park, H., Liu, Y., Solis, N. V., Spotkov, J., Hamaker, J. J., Blankenship, J. R., Yeaman, M. R., Mitchell, A. P., Liu, H., & Filler, S. G. (2009) · Eukaryotic Cell · doi:10.1128/ec.00165-09 · Cited by 59
“Strain CAI4-URA, which was originally derived from the clinical isolate SC5314 (59), was used as the reference strain, and its response to both oral epithelial cells and endothelial cells was determined.”
BackgroundMethodInfluentialSelf-citationCandida albicans protein kinase CK2 governs virulence during oropharyngeal candidiasis
Chiang, L. Y., Sheppard, D. C., Bruno, V. M., Mitchell, A. P., Edwards, J. E., & Filler, S. G. (2007) · Cellular Microbiology · doi:10.1111/j.1462-5822.2006.00784.x · Cited by 59
“The endothelial cell damage defect and attenuated virulence of the mds3 insertion mutant in the mouse model of haematogenously disseminated candidiasis have been reported previously (Sanchez et al., 2004).”
BackgroundMethodInfluentialSelf-citationVonk, A. G., Netea, M. G., van der Meer, J. W. M., & Kullberg, B. J. (2006) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.6.9.891 · Cited by 54
“albicans factors other than the ability to form long hyphae may be necessary for the organism to damage endothelial cells [22].”
BackgroundDesai, C., Mavrianos, J., & Chauhan, N. (2011) · FEMS Yeast Research · doi:10.1111/j.1567-1364.2011.00743.x · Cited by 52
“In a screen for mutants defective in damage to endothelial cell, Sanchez et al (2004) reported that C. albicans mutants, which caused less damage to endothelial cells, were also less virulent in a mouse model of disseminated candidiasis.”
BackgroundAnimal models in the analysis of Candida host–pathogen interactions
de Repentigny, L. (2004) · Current Opinion in Microbiology · doi:10.1016/j.mib.2004.06.001 · Cited by 69
Lagree, K., Woolford, C. A., Huang, M. Y., May, G. E., McManus, C. J., Solis, N. V., Filler, S. G., & Mitchell, A. P. (2020) · PLoS Genetics · doi:10.1371/journal.pgen.1008582 · Cited by 55
“We also assayed host cell interaction through the ability of the mutant strains to cause endothelial cell damage [50], using primary human umbilical vein endothelial cells.”
BackgroundSelf-citationFungicidal and Cytotoxic Activity of a Capsicum chinense Defensin Expressed by Endothelial Cells
Anaya-López, J. L., López-Meza, J. E., Baizabal-Aguirre, V. M., Cano-Camacho, H., & Ochoa‐Zarzosa, A. (2006) · Biotechnology Letters · doi:10.1007/s10529-006-9060-4 · Cited by 51
“Adhesion, invasion and damage of C. albicans to endothelial cells have been demonstrated using in vivo and in vitro models (Jong et al. 2001; Sánchez et al. 2004).”
MethodRole of Arf GTPases in fungal morphogenesis and virulence
Labbaoui, H., Bogliolo, S., Ghugtyal, V., Solis, N. V., Filler, S. G., Arkowitz, R. A., & Bassilana, M. (2017) · PLoS Pathogens · doi:10.1371/journal.ppat.1006205 · Cited by 51
“To induce haematogenously disseminated candidiasis (HDC), 8 Balb/C mice per strain were injected via the tail vein with an inoculum of 5x10(5) cells [83].”
Self-citationNisin Z inhibits the growth ofCandida albicansand its transition from blastospore to hyphal form
Lay, C., Akerey, B., Fliss, I., Subirade, M., & Rouabhia, M. (2008) · Journal of Applied Microbiology · doi:10.1111/j.1365-2672.2008.03908.x · Cited by 47
“Host cell invasion and damage are likely critical virulence attributes of C. albicans (Phan et al. 2000; Sanchez et al. 2004; Park et al. 2005; Chiang et al. 2007).”
BackgroundSeman, B. G., Moore, J. L., Scherer, A. K., Blair, B. A., Manandhar, S., Jones, J. M., & Wheeler, R. T. (2018) · Infection and Immunity · doi:10.1128/iai.00415-18 · Cited by 50
“This enabled noninvasive quantification of morphology, invasion, yeast proliferation, and dissemination frequency; of these, only invasion has been quantified in vitro previously, through damage assays (56).”
BackgroundIn vitroinfection models to study fungal–host interactions
Last, A., Maurer, M., Mosig, A. S., Gresnigt, M. S., & Hube, B. (2021) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuab005 · Cited by 45
Owais, M., Khan, A. A., Zubair, S., & Zia, Q. (2015) · International Journal of Nanomedicine · doi:10.2147/ijn.s63155 · Cited by 44
“96,97 A reduction in hyphal content as well as lower fungal viability (Figures 8 and 9) makes the AmB−PGA nanoformulation a promising strategy for dealing with bio-films.”
Candida albicans: Molecular interactions with Pseudomonas aeruginosa and Staphylococcus aureus
Lindsay, A. K., & Hogan, D. A. (2014) · Fungal Biology Reviews · doi:10.1016/j.fbr.2014.10.002 · Cited by 45
Transcriptome Profile of the Vascular Endothelial Cell Response toCandida albicans
Barker, K. S., Park, H., Phan, Q. T., Xu, L., Homayouni, R., Rogers, P. D., & Filler, S. G. (2008) · The Journal of Infectious Diseases · doi:10.1086/589516 · Cited by 44
“albicans induces significant EC damage (figure 1B) [4, 5, 8, 13], thus, it was interesting that the genes related to the response to stress or wounding were overrepresented in response to SC5314 (table 1).”
BackgroundSelf-citationPeroumal, D., Sahu, S. R., Kumari, P., Utkalaja, B. G., & Acharya, N. (2022) · Microbiology Spectrum · doi:10.1128/spectrum.02462-22 · Cited by 40
“albicans: additionally, it requires immunosuppression of the host and damage to the mucosal layer (13).”
BackgroundSR-Like RNA-Binding Protein Slr1 Affects Candida albicans Filamentation and Virulence
Ariyachet, C., Solis, N. V., Liu, Y., Prasadarao, N. V., Filler, S. G., & McBride, A. E. (2013) · Infection and Immunity · doi:10.1128/iai.00864-12 · Cited by 39
“Therefore, the impaired growth of the slr1 / mutant likely played a minor role in its reduced virulence in the mouse model of HDC.”
BackgroundInfluentialSelf-citationSSD1 Is Integral to Host Defense Peptide Resistance in Candida albicans
Gank, K. D., Yeaman, M. R., Kojima, S., Yount, N. Y., Park, H., Edwards, J. E., Filler, S. G., & Fu, Y. (2008) · Eukaryotic Cell · doi:10.1128/ec.00402-07 · Cited by 37
“3 ml of phosphate-buffered saline (31).”
BackgroundMethodInfluentialSelf-citationFungal complications afterCandidapreservation fluid contamination in liver transplant recipients
Levesque, É., Paugam‐Burtz, C., Saliba, F., Khoy-Ear, L., Merle, J., Jung, B., Stecken, L., Ferrandière, M., Mihaïla-Amrouche, L., & Botterel, F. (2015) · Transplant International · doi:10.1111/tri.12633 · Cited by 36
“endothelial cells, leading to the destruction of vascular structures [21,22].”
BackgroundFunctional diversification accompanies gene family expansion of MED2 homologs in Candida albicans
Dunn, M. J., Kinney, G. M., Washington, P. M., Berman, J. G., & Anderson, M. Z. (2018) · PLoS Genetics · doi:10.1371/journal.pgen.1007326 · Cited by 36
Seidl, K., Bayer, A. S., McKinnell, J. A., Ellison, S., Filler, S. G., & Xiong, Y. Q. (2011) · Cellular Microbiology · doi:10.1111/j.1462-5822.2011.01639.x · Cited by 33
“Candida albicans and Aspergillus fumigatus (Sanchez et al., 2004; Chiang et al., 2008).”
BackgroundSelf-citationSeidl, K., Solis, N. V., Bayer, A. S., Abdelhady, W., Ellison, S., Klashman, M., Xiong, Y. Q., & Filler, S. G. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039633 · Cited by 33
“aureus to damage HUVECs in vitro is directly correlated with their virulence in animal models of hematogenous infection [13,14].”
BackgroundMethodSelf-citationCandida Infections and Modelling Disease
MacCallum, D. M. (2009) · Springer eBooks · doi:10.1007/978-3-642-03150-2_3 · Cited by 30
Candida arteritis in kidney transplant recipients: case report and review of the literature
Dębska-Ślizień, A. M., Chrobak, Ł., Bzoma, B., Perkowska, A., Zadrożny, D., Chamienia, A. L., Kostro, J., Milecka, A., Bronk, M., Śledziński, Z., et al. (2015) · Transplant Infectious Disease · doi:10.1111/tid.12388 · Cited by 30
“The reasons why some cases of Candida contamination led to mycotic arteritis, while others did not, are not clear, although differences in Candida virulence that determine its capacity to penetrate endothelial cells may be one explanation (13).”
BackgroundRole of Aspergillus fumigatus DvrA in Host Cell Interactions and Virulence
Ejzykowicz, D. E., Solis, N. V., Gravelat, F. N., Chabot, J. C., Li, X., Sheppard, D. C., & Filler, S. G. (2010) · Eukaryotic Cell · doi:10.1128/ec.00055-10 · Cited by 30
“albicans strains to damage endothelial cells in vitro is a fairly good predictor of their virulence in the mouse model of disseminated candidiasis (32).”
BackgroundSelf-citationJung, S., Rodriguez, N. S., Irrizary, J., Liboro, K., Bogarin, T., Macias, M., Eivers, E., Porter, E. M., Filler, S. G., & Park, H. (2017) · PLoS ONE · doi:10.1371/journal.pone.0187721 · Cited by 34
Self-citationSen, M., Shah, B., Rakshit, S., Singh, V., Padmanabhan, B., Ponnusamy, M., Pari, K., Vishwakarma, R. A., Nandi, D., & Sadhale, P. P. (2011) · PLoS Pathogens · doi:10.1371/journal.ppat.1002384 · Cited by 25
“locus. This is consistent with earlier reports that the DAY286 strain is ∼70% as virulent as compared to SC5314”
ResultCandida Species Contamination of Preservation Fluid—Outcome of Renal Transplantation in 6 Patients
Rodrigues, B. F., Natário, A., Vizinho, R., Jorge, C. R. D. F. M., Weigert, A. L. L., Martinho, A., Toscano, C., Marques, T. T., & Machado, D. (2013) · Transplantation Proceedings · doi:10.1016/j.transproceed.2013.03.024 · Cited by 25
“This phenomenon may be explained by the ability of C albicans to adhere, invade, and damage human vascular endothelial cells.(24,25) Our affected patients showed clinical presentations similar to those previously described in the literature: some patients have an abrupt onset with hypovolemic shock requiring emergency…”
ResultAdhesins in Opportunistic Fungal Pathogens
Zordan, R. E., & Cormack, B. P. (2014) · ASM Press eBooks · doi:10.1128/9781555817176.ch16 · Cited by 24
Li, S.-X., Song, Y.-J., Zhang, Y.-S., Wu, H.-T., Guo, H., Zhu, K.-J., Li, D.-M., & Zhang, H. (2017) · Frontiers in Microbiology · doi:10.3389/fmicb.2017.00285 · Cited by 25
“Shake cultures were grown at 30◦C and OD600 of each strain was measured every two hours.”
BackgroundMethodCanaud, G., Timsit, M., Zuber, J., Bougnoux, M., Méjean, A., Thervet, É., Snanoudj, R., Sberro‐Soussan, R., Martinez, F., Legendre, C., et al. (2008) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfn622 · Cited by 24
“albicans, has the ability to penetrate endothelial cells and lead to arteritis [3,4].”
BackgroundAlarmin(g) the innate immune system to invasive fungal infections
Caffrey, A. K., & Obar, J. J. (2016) · Current Opinion in Microbiology · doi:10.1016/j.mib.2016.06.002 · Cited by 22
Characterization of carboxylate nanoparticle adhesion with the fungal pathogen Candida albicans
Lyden, A., Lombardi, L., Sire, W., Li, P., Simpson, J. C., Butler, G., & Lee, G. U. (2017) · Nanoscale · doi:10.1039/c7nr04724j · Cited by 21
Cryopreserved Venous Allografts in Supra-inguinal Reconstructions: A Single Centre Experience
Heinola, I., Kantonen, I., Mattila, I. P., Albäck, A., & Venermo, M. A. (2019) · European Journal of Vascular and Endovascular Surgery · doi:10.1016/j.ejvs.2019.06.024 · Cited by 19
Hgc1 Independence of Biofilm Hyphae in Candida albicans
Sharma, A., Solis, N. V., Huang, M. Y., Lanni, F., Filler, S. G., & Mitchell, A. P. (2023) · mBio · doi:10.1128/mbio.03498-22 · Cited by 18
“Because hyphal defects are associated with endothelial cell damage defects (4, 27), these results are consistent with current understanding of Hgc1 function.”
ResultSelf-citationBasante-Bedoya, M. A., Bogliolo, S., García‐Rodas, R., Zaragoza, Ó., Arkowitz, R. A., & Bassilana, M. (2022) · PLoS Genetics · doi:10.1371/journal.pgen.1010549 · Cited by 18
Functional Dichotomy for a Hyphal Repressor in Candida albicans
Mao, Y., Solis, N. V., Filler, S. G., & Mitchell, A. P. (2023) · mBio · doi:10.1128/mbio.00134-23 · Cited by 17
“albicans for 3 h, after which the extent of host cell damage was determined using a (51)Cr release assay, following standard methods (21).”
BackgroundMethodSelf-citationToward a Molecular Understanding ofCandida albicansVirulence
Odds, F. C., Gow, N. A. R., & Brown, A. J. P. (2014) · ASM Press eBooks · doi:10.1128/9781555815776.ch22 · Cited by 18
Levesque, É., Suet, G., Merle, J., Compagnon, P., Amathieu, R., Féray, C., Botterel, F., Foulet, F., Azoulay, D., & Dhonneur, G. (2014) · Transplant Infectious Disease · doi:10.1111/tid.12260 · Cited by 17
“albicans, to penetrate into endothelial cells leading to destruction of vascular structures (11).”
BackgroundZhou, X., Hilk, A. L., Solis, N. V., de Sá, N. P., Hogan, B. M., Bierbaum, T. A., Poeta, M. D., Filler, S. G., Burrack, L. S., & Selmecki, A. M. (2024) · PLoS Pathogens · doi:10.1371/journal.ppat.1012389 · Cited by 18
Self-citationPharmacokinetics of Murine p75-Fc Fusion Protein and MP6-XT22 Anti-Murine TNF-α mAb in Mice
Filler, S. G., Solis, N. V., Guo, J., Doellgast, G. J., Ruiz-Garcı́a, A., & Pan, W. (2007) · Journal of Investigative Dermatology Symposium Proceedings · doi:10.1038/sj.jidsymp.5650036 · Cited by 15
Self-citationStaniszewska, M., Bondaryk, M., Malewski, T., & Schaller, M. (2014) · Open Life Sciences · doi:10.2478/s11535-014-0311-4 · Cited by 14
García‐Rodas, R., Labbaoui, H., Orange, F., Solis, N. V., Zaragoza, Ó., Filler, S. G., Bassilana, M., & Arkowitz, R. A. (2022) · mBio · doi:10.1128/mbio.03873-21 · Cited by 13
“HDC was induced in 10 BALB/c mice (Charles River, Italy) per group by injecting the lateral tail vein with an inoculum of 5 10(5) cells (59).”
MethodSelf-citationPark, H., Solis, N. V., Louie, J. S., Spellberg, B., Rodriguez, N., & Filler, S. G. (2014) · Virulence · doi:10.4161/viru.29699 · Cited by 11
Self-citationNeonatal candidiasis in Venezuela: clinical and epidemiological aspects.
de Capriles, C. H., Mata‐Essayag, S., Azpiróz, A., Ponente, A., Magaldi, S., Pérez, C., Roselló, A., Colella, M. T., & Machuca, J. (2005) · PubMed · Cited by 11
Use of the Iron-Responsive RBT5 Promoter for Regulated Expression in Candida albicans
Mao, Y., Solis, N. V., Sharma, A., Cravener, M. V., Filler, S. G., & Mitchell, A. P. (2022) · mSphere · doi:10.1128/msphere.00305-22 · Cited by 10
Self-citationSerum bridging molecules drive candidal invasion of human but not mouse endothelial cells
Phan, Q. T., Solis, N. V., Lin, J., Swidergall, M., Singh, S., Liu, H., Sheppard, D. C., Ibrahim, A. S., Mitchell, A. P., & Filler, S. G. (2022) · PLoS Pathogens · doi:10.1371/journal.ppat.1010681 · Cited by 10
“When wild-type C . albicans is endocytosed by endothelial cells, it damages these cells, likely by releasing candidalysin into the invasion pocket [6,29–31].”
Self-citationHost albumin redirects Candida albicans metabolism to engage an alternative pathogenicity pathway
Hitzler, S. U. J., Fernández-Fernández, C., Günther, K., Dietschmann, A., Hovhannisyan, H., Möslinger, A., Austermeier, S., Cristóvão, B., Vascelli, G., Zelante, T., et al. (2025) · Nature Communications · doi:10.1038/s41467-025-61701-5 · Cited by 9
Yang, C., Li, G., Zhang, Q., Bai, W., Li, Q., Zhang, P., & Zhang, J. (2024) · mBio · doi:10.1128/mbio.00445-24 · Cited by 8
“The virulence of the various strains was tested in the mouse model of hematogenously disseminated candidiasis as described previously (50).”
BackgroundA novel renal epithelial cell in vitro assay to assessCandida albicansvirulence
Szabo, E. K., & MacCallum, D. M. (2013) · Virulence · doi:10.4161/viru.27046 · Cited by 6
“The escape of fungi from the bloodstream during systemic candidiasis has been modeled in vitro using endothelial cells.(28-30,53) Endothelial cell damage and cytokine production was induced only by live, germinated fungal cells,(53) and those C.”
BackgroundInfluentialMolecular Basis of Fungal Adherence to Endothelial and Epithelial Cells
Filler, S. G., Sheppard, D. C., & Edwards, J. E. (2014) · ASM Press eBooks · doi:10.1128/9781555815776.ch13 · Cited by 5
Self-citationZhou, X., Hilk, A. L., Solis, N. V., Hogan, B. M., Bierbaum, T. A., Filler, S. G., Burrack, L. S., & Selmecki, A. M. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.03.06.583770 · Cited by 5
Self-citationMacrophage-derived CD36 + exosome subpopulations as novel biomarkers of Candida albicans infection
Li, S., Xv, Y., Sun, Y., Shen, Z., Hao, R., Yan, J., Liu, M., Liu, Z., Jing, T., Li, X., et al. (2024) · Scientific Reports · doi:10.1038/s41598-024-60032-7 · Cited by 4
“Endocytosis mediated by endothelial cells via N-cadherin plays a role in the internalization of C. albicans 28 , which can subsequently escape through vesicle phagocytosis or endothelial cell loss 29 .”
BackgroundSamaranayake, D., Atencio, D. P., Morse, R. H., Wade, J. T., Chaturvedi, V. P., & Hanes, S. D. (2013) · PLoS ONE · doi:10.1371/journal.pone.0059094 · Cited by 5
“The CAI4 (ura(2)) parent strain is a poorly-filamenting strain, presumably due to its uracil auxotrophy [60].”
BackgroundEncounters with Mammalian Cells: Survival Strategies ofCandidaSpecies
Vylkova, S., & Lorenz, M. C. (2014) · ASM Press eBooks · doi:10.1128/9781555817176.ch17 · Cited by 5
Shining a light on Candida -induced epithelial damage with a luciferase reporter
Tesfamariam, M., Vij, R., Trümper, V., Hube, B., & Brunke, S. (2024) · mSphere · doi:10.1128/msphere.00509-24 · Cited by 3
“Methods like detection of LDH release (6, 7), release of radiolabeled chromium ( 51 Cr) (8, 9), and fluorescence microscopy of propidium iodide (PI)-stained nuclei of dying cells (10), have all been used in the past with great success, for example, in the discovery of the fungal peptide toxin…”
Molecular Pathogenesis of Fungal Infections
Segal, B. H. (2007) · Humana Press eBooks · doi:10.1007/978-1-59259-963-9_95 · Cited by 3
Matignon, M., Botterel, F., Audard, V., Dunogué, B., Dahan, K., Lang, P., Bretagne, S., & Grimbert, P. (2008) · American Journal of Transplantation · doi:10.1111/j.1600-6143.2007.02092.x · Cited by 2
Innate and Adaptive Immunity to Systemic Candida albicans Infection
Romani, L. R. (2005) · Springer eBooks · doi:10.1007/0-387-25445-5_19 · Cited by 2
Candida graft arteritis after kidney transplantation: two cases and literature review
Kumar, T. P., Prabhu, R., Kiran, P., Chawla, A. K., Priya, P. S., Singh, B. M. K., & Gupta, N. R. (2025) · Oxford Medical Case Reports · doi:10.1093/omcr/omaf172 · Cited by 1
“Its phospholipase activity and stimulation of prostaglandin production contribute to endothelial injury [21, 22].”
In vitro models of hematogenously disseminated candidiasis
Filler, S. G. (2014) · Virulence · doi:10.4161/viru.27453 · Cited by 1
“The correlation between host cell damage and virulence has been demonstrated most clearly using the human umbilical vein endothelial cell model.(19,36-38) However, some mutant strains have significantly impaired capacity to damage endothelial cells in vitro, yet have normal or even increased virulence during dissemina…”
BackgroundSelf-citationIn vitro models to analyse fungal infection
Gola, S., Arana, D. M., Alonso‐Monge, R., Román, E., & Plá, J. (2007) · Springer eBooks · doi:10.1007/978-1-4020-6397-8_2 · Cited by 1
Phan, Q., Solis, N., Lin, J., Swidergall, M., Singh, S., Liu, H., Sheppard, D., Ibrahim, A., Mitchell, A., & Filler, S. (2021) · bioRxiv · doi:10.1101/2021.09.18.460925 · Cited by 1
“likely by releasing candidalysin into the invasion pocket (6, 29-31).”
BackgroundSelf-citationInteractions of Fungi with Endothelial Cells
Filler, S. G., & Sheppard, D. C. (2005) · Springer eBooks · doi:10.1007/0-387-25445-5_20
“Other multiple mutants of C. albicans have been identified that have reduced capacity to injure endothelial cells (Davis et al., 2000; Phan et al., 2000; Bensen et al., 2002; Blankenship et al., 2003; Sanchez et al., 2004 ).”
BackgroundResultSelf-citationCandida Albicans: New Insights in Infection, Disease, and Treatment
MacCallum, D. M. (2007) · Springer eBooks · doi:10.1007/978-1-4020-6397-8_5
MINIREVIEWS Glucose Sensing Network in Candida albicans: a Sweet Spot for Fungal Morphogenesis
Sabina, J., & Brown, V. E. (2009)
Metadata
- Authors
- Sanchez, A. A., Johnston, D. A., Myers, C., Edwards, J. E., Mitchell, A. P., & Filler, S. G.
- Affiliations
- University of California, Los Angeles (US)
- Columbia University (US)
- Corresponding author
- Filler, Scott G.
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2004-01
- Volume
- 72
- Issue
- 1
- Pages
- 598-601
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC344013
- OpenAlex
- W2133054734
- Cited by
- 101
- References
- 36
- Citations by year
- 2025: 2 · 2024: 5 · 2023: 2 · 2022: 5 · 2021: 2 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 1 · 2015: 6 · 2014: 11 · 2013: 5 · 2012: 5
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (P01 AI-37194, R29AI040636, R01AI019990, R01AI050931, R01-AI19990, R01 AI 50931, P01AI037194)
- National Institute of Dental and Craniofacial Research (R01DE013974, R01 DE 13974)
- National Center for Research Resources (M01RR000425, M01-RR00425)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Infectious Diseases › Fungal Infections and Studies
- Keywords
- Candida albicans, virulence factors, endothelial injury, fungal mutants
- MeSH terms
- Animals, Candida albicans, Candidiasis, Cytotoxicity Tests, Immunologic, Endothelium, Vascular, Male, Mice, Inbred BALB C, Mutation, Umbilical Cord, Virulence, Virulence Factors, Endothelial Cells, Mice
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