The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Role of Hyphal Formation in Interactions of Candida albicans with Endothelial Cells
Open accessAbstract
The ability to change from yeast to hyphal morphology is a major virulence determinant of Candida albicans . Mutants with defined defects in filamentation regulatory pathways have reduced virulence in mice. However, is it poorly understood why hyphal formation is critical for C. albicans to cause hematogenously disseminated infections. We used recently constructed mutants to examine the role of hyphal formation in the interactions of C. albicans with endothelial cells in vitro. These interactions included the ability of the mutants to invade and injure endothelial cells. Because the formation of hyphae may influence the host inflammatory response to C. albicans , we also investigated the capacity of these mutants to stimulate endothelial cells to express E-selectin and intercellular adhesion molecule 1. We infected endothelial cells with C. albicans strains containing homozygous null mutations in the following filamentation regulatory genes: CLA4 , CPH1 , EFG1 , and TUP1 . Whereas the wild-type strain formed true hyphae on endothelial cells, we found that neither the Δ efg1 nor the Δ cph1 Δefg1 double mutant germinated. The Δ tup1 mutant formed only pseudohyphae. We also found that the Δ efg1 , Δ cph1 Δefg1 , and Δ tup1 mutants had significantly reduced capacities to invade and injure endothelial cells. Therefore, Efg1p and Tup1p contribute to virulence by regulating hyphal formation and the factors that enable C. albicans to invade and injure endothelial cells. With the exception of the Δcph1 Δefg1 mutant, all other mutants stimulated endothelial cells to express at least one of the leukocyte adhesion molecules. Therefore, the combined activities of Cph1p and Efg1p are required for C. albicans to stimulate a proinflammatory response in endothelial cells.
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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 [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Furthermore, studies with killed organisms indicate that induction of endocytosis is passive on the part of the organism because killed hyphae are endocytosed as avidly as are live hyphae [5,7].”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Previously, we have found that C. albicans invades both endothelial cells and oral epithelial cells in vitro by inducing its own endocytosis [4,5,7].”
From Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells (2007) · cites this paper as [7]
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Citations
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Cited by
Sorted by citations
Saville, S. P., Lazzell, A. L., Monteagudo, C., & Lopez-Ribot, J. L. (2003) · Eukaryotic Cell · doi:10.1128/ec.2.5.1053-1060.2003 · Cited by 655
“It has been assumed that these few infecting cells had somehow managed to form filaments in vivo through an Efg1p/Cph1p-independent mechanism, possibly through activation of the transcription factor Czf1p (8, 12), which had enabled them to extravasate and disseminate to the organs, with supporting evidence for this pr…”
BackgroundAls3 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
“Furthermore, studies with killed organisms indicate that induction of endocytosis is passive on the part of the organism because killed hyphae are endocytosed as avidly as are live hyphae [5,7].”
BackgroundMethodSelf-citationOral Candidiasis: A Disease of Opportunity
Vila, T., Sultan, A. S., Montelongo-Jauregui, D., & Jabra-Rizk, M. A. (2020) · Journal of Fungi · doi:10.3390/jof6010015 · Cited by 537
Candida albicans Cell Wall Proteins
Chaffin, W. L. (2008) · Microbiology and Molecular Biology Reviews · doi:10.1128/mmbr.00032-07 · Cited by 515
Fradin, C., De Groot, P., MacCallum, D., Schaller, M., Klis, F., Odds, F. C., & Hube, B. (2005) · Molecular Microbiology · doi:10.1111/j.1365-2958.2005.04557.x · Cited by 455
“…to adhere to endothelial cells (Rotrosen et al., 1985) and hyphal cells, but not yeast cells, have been shown to induce phagocytosis by endothelial cells, a mechanism which is discussed as a potential strategy of C. albicans to escape from the bloodstream (Zink et al., 1996; Phan et al., 2000).”
Background
Metadata
- Authors
- Phan, Q. T., Belanger, P. H., & Filler, S. G.
- Affiliations
- University of California, Los Angeles (US)
- ORCID
- Filler, Scott G.
- Venue
- Infection and Immunity
- Publisher
- American Society for Microbiology
- Published
- 2000-06
- Volume
- 68
- Issue
- 6
- Pages
- 3485-3490
- ISSN
- 0019-9567 (ISSN-L)
- 1098-5522
- PMC
- PMC97632
- OpenAlex
- W2134152581
- Cited by
- 181
- References
- 31
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 4 · 2021: 4 · 2020: 6 · 2019: 2 · 2018: 8 · 2017: 4 · 2016: 4 · 2015: 6 · 2014: 13 · 2013: 7 · 2012: 7
- FWCI
- 6.28
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Infection and Immunity (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Burroughs Wellcome Fund
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (P01 AI-37194, R29AI040636, R01AI019990, R01-AI19990, P01AI037194)
- National Center for Research Resources (M01RR000425)
- 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, hyphal development, filamentation, endothelial cells, pseudohyphae, endothelial cell invasion, leukocyte adhesion molecules, E-selectin, ICAM-1, inflammation, virulence, yeast-to-hypha transition
- MeSH terms
- Candida albicans, DNA-Binding Proteins, Endocytosis, Endothelium, Vascular, Fungal Proteins, Genes, Fungal, Humans, Morphogenesis, Mutation, Nuclear Proteins, Repressor Proteins, Transcription Factors, Protein Serine-Threonine Kinases, Intercellular Adhesion Molecule-1, E-Selectin, Saccharomyces cerevisiae Proteins
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