The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index.
Role of Bcr1-Activated Genes Hwp1 and Hyr1 in Candida Albicans Oral Mucosal Biofilms and Neutrophil Evasion
Open accessAbstract
Candida albicans triggers recurrent infections of the oropharyngeal mucosa that result from biofilm growth. Prior studies have indicated that the transcription factor Bcr1 regulates biofilm formation in a catheter model, both in vitro and in vivo. We thus hypothesized that Bcr1 plays similar roles in the formation of oral mucosal biofilms and tested this hypothesis in a mouse model of oral infection. We found that a bcr1/bcr1 mutant did not form significant biofilm on the tongues of immunocompromised mice, in contrast to reference and reconstituted strains that formed pseudomembranes covering most of the tongue dorsal surface. Overexpression of HWP1, which specifies an epithelial adhesin that is under the transcriptional control of Bcr1, partly but significantly rescued the bcr1/bcr1 biofilm phenotype in vivo. Since HWP1 overexpression only partly reversed the biofilm phenotype, we investigated whether additional mechanisms, besides adhesin down-regulation, were responsible for the reduced virulence of this mutant. We discovered that the bcr1/bcr1 mutant was more susceptible to damage by human leukocytes when grown on plastic or on the surface of a human oral mucosa tissue analogue. Overexpression of HYR1, but not HWP1, significantly rescued this phenotype. Furthermore a hyr1/hyr1 mutant had significantly attenuated virulence in the mouse oral biofilm model of infection. These discoveries show that Bcr1 is critical for mucosal biofilm infection via regulation of epithelial cell adhesin and neutrophil function.
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“This hyphal-specific protein has previously been found to inhibit C. albicans killing by neutrophils and contribute to virulence in mouse models of both disseminated candidiasis and OPC, but its host cell receptor was unknown [24,25].”
From Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection (2023) · cites this paper as [25]
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“It has previously been found that Hyr1 also required for maximal virulence in an immunosuppressed mouse model of OPC [25].”
From Candida albicans stimulates formation of a multi-receptor complex that mediates epithelial cell invasion during oropharyngeal infection (2023) · cites this paper as [25]
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Cites
Single-Step Method of RNA Isolation by Acid Guanidinium Thiocyanate–Phenol–Chloroform Extraction
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Als3 Is a Candida albicans Invasin That Binds to Cadherins and Induces Endocytosis by Host Cells
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Critical Role of Bcr1-Dependent Adhesins in C. albicans Biofilm Formation In Vitro and In Vivo
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Self-citationRegulation of Cell-Surface Genes and Biofilm Formation by the C. albicans Transcription Factor Bcr1p
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Self-citationFradin, 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
Function of Candida albicans Adhesin Hwp1 in Biofilm Formation
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Self-citationJesaitis, A. J., Franklin, M. J., Berglund, D. L., Sasaki, M., Lord, C. I., Bleazard, J. B., Duffy, J. E., Beyenal, H., & Lewandowski, Z. (2003) · The Journal of Immunology · doi:10.4049/jimmunol.171.8.4329 · Cited by 373
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Candida albicans forms biofilms on the vaginal mucosa
Harriott, M. M., Lilly, E. A., Rodriguez, T. E., Fidel, P. L., & Noverr, M. C. (2010) · Microbiology · doi:10.1099/mic.0.039354-0 · Cited by 301 · cited 3×
“with results in the mouse vaginal mucosa model [16], we found that the bcr1/bcr1 strain was deficient in forming a clinically visible mucosal biofilm on the tongues of immunocompromised mice in vivo (Fig.”
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Lilly, A. J., Fidel, P. L., Noverr, M. C., Peters, B. M., Palmer, G. E., & Nash, A. K. (2014)
Monroy, G. L. (2018) · Illinois Digital Environment for Access to Learning and Scholarship (University of Illinois at Urbana-Champaign)
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Solis, N. V., Wakade, R. S., Ollinger, T. L., Wellington, M. A., Mitchell, A. P., Filler, S. G., & Krysan, D. J. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.05.24.445409
Self-citationMetabolomic study of biofilm-forming natural microbiota of skin biofilm
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Biernasiuk, A., Ostrowska-Leśko, M., Malm, A., & Korga-Plewko, A. (2026) · Journal of Oral Microbiology · doi:10.1080/20002297.2026.2741862
Metadata
- Authors
- Dwivedi, P., Thompson, A., Xie, Z., Kashleva, H., Ganguly, S., Mitchell, A. P., & Dongari-Bagtzoglou, A.
- Affiliations
- University of Connecticut (US)
- Carnegie Mellon University (US)
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2011-01-25
- Volume
- 6
- Issue
- 1
- Pages
- e16218
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3026825
- OpenAlex
- W2091452473
- Cited by
- 110
- References
- 42
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 10 · 2023: 11 · 2022: 5 · 2021: 6 · 2020: 2 · 2019: 6 · 2018: 8 · 2017: 12 · 2016: 7 · 2015: 4 · 2014: 6 · 2013: 9 · 2012: 12
- FWCI
- 6.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01AI067703)
- National Institute of Dental and Craniofacial Research (R01DE013986)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bacterial biofilms and quorum sensing
- Keywords
- Candida albicans, HWP1, fungal virulence, oropharyngeal infection, immunodeficient mice, pseudomembranous candidiasis
- MeSH terms
- Animals, Candida albicans, Fungal Proteins, Membrane Glycoproteins, Mouth Mucosa, Neutrophils, Transcription Factors, Biofilms, Adhesins, Bacterial, Mice, Immune Evasion
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