Adherence of Candida to Cultured Vascular Endothelial Cells: Mechanisms of Attachment and Endothelial Cell Penetration
Abstract
To elucidate the pathogenesis of hematogenous Candida infections, we developed an in vitro model of Candida adherence to and penetration of human endothelial cells. We enhanced or inhibited adherence in order to probe mechanisms of attachment. Adherence of Candida albicans showed a linear relation to Candida inoculum (range, 10(2)-10(5) cfu, r = .99, P less than .01) and exceeded that of less virulent Candida species and that of Saccharomyces cerevisiae (P less than .01). Candida immune serum blocked attachment (greater than 95% inhibition; P less than .001), however, this activity was abolished by immunoprecipitation of immune serum with C. albicans mannan (P less than .001) and was unaffected by immunoprecipitation with S. cerevisiae mannan or by adsorption with particulate chitin. Adherence was diminished by exposing C. albicans to heat (greater than 99% inhibition; P less than .01), UV light (98% inhibition; P less than .01), or sodium periodate (greater than 72% inhibition; P less than .01). An extract from heat-exposed C. albicans blocked adherence (greater than 51% inhibition; P less than .001). Transmission electron microscopy demonstrated that viable or killed Candida organisms were attached to endothelial cells, were enveloped by membrane processes from the endothelial cell surface, and were incorporated into the endothelial cells within phagosomes. Cytochalasin B blocked incorporation without blocking surface attachment.
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Infection of endothelial cells or oral epithelial cells with wild-type C. albicans hyphae in vitro causes significant damage to these cells, and endocytosis of the organisms is required to induce host cell damage.
“Infection of endothelial cells or oral epithelial cells with wild-type C. albicans hyphae in vitro causes significant damage to these cells, and endocytosis of the organisms is required to induce host cell damage [4,5,10].”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [10]
Endothelial cell endocytosis of C. albicans is induced when the organism binds to N-cadherin and other endothelial cell surface proteins.
“Endothelial cell endocytosis of C. albicans is induced when the organism binds to N-cadherin and other endothelial cell surface proteins.”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [10]
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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 · see citing works
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Candida albicans Als3, a multifunctional adhesin and invasin
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Host Cell Invasion and Virulence Mediated by Candida albicans Ssa1
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Penetration and damage of endothelial cells by Candida albicans
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<i>Candida albicans</i>internalization by host cells is mediated by a clathrin-dependent mechanism
Moreno-Ruiz, E., Galán-Díez, M., Zhu, W., Fernández-Ruiz, E., d'Enfert, C., Filler, S. G., Cossart, P., & Veiga, E. (2009) · Cellular Microbiology · doi:10.1111/j.1462-5822.2009.01319.x · Cited by 133 · see citing works
N-cadherin Mediates Endocytosis of Candida albicans by Endothelial Cells
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Self-citationMechanisms 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 · see citing works
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Torres-Tirado, D., Knabb, M., Castaño, I., Patrón-Soberano, A., De Las Peñas, A., & Rubio, R. (2016) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00229.2014 · Cited by 10 · see citing works
- Authors
- Rotrosen, D., Edwards, J. E., Gibson, T. R., Moore, J. C., Cohen, A. H., & Green, I.
- Venue
- Journal of Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 1985-12-01
- Volume
- 152
- Issue
- 6
- Pages
- 1264-1274
- ISSN
- 0022-1899 (ISSN-L)
- 1537-6613
- OpenAlex
- W2134690832
- Cited by
- 146
- References
- 1
- Citations by year
- 2019: 1 · 2017: 3 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 1
- FWCI
- 8.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Infectious Diseases (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI 06946, AI-19990)
- 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 › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, endothelial cells, mannan, antisera, phagocytosis, cytochalasin B, virulence, sodium periodate, Saccharomyces cerevisiae
- MeSH terms
- Adhesiveness, Animals, Antifungal Agents, Aorta, Candida albicans, Endothelium, Female, Humans, Immune Sera, Microscopy, Electron, Scanning, Rabbits, Saccharomyces cerevisiae, Spores, Fungal, Time Factors, Umbilical Veins
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