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Article: Candida albicans Secreted Aspartic Protease 7 is Essential for Damage of Human Oral Epithelial Cells

TitleCandida albicans Secreted Aspartic Protease 7 is Essential for Damage of Human Oral Epithelial Cells
Authors
KeywordsCandida albicans
Secreted aspartic protease
Oral epithelial cells
Endocytosis
Tissue damage
Issue Date2021
PublisherAustin Publishers.
Citation
Journal of Bacteriology and Mycology, 2021, v. 8 n. 5 How to Cite?
AbstractAims: Candida albicans is an important human fungal pathogen in clinical settings. It possesses a wide spectrum of virulence traits, including but not limited to the production of Secreted Aspartic Proteases (SAPs), to invade host cells under predisposing conditions. The aims of the present study were to investigate the functional role of C. albicans SAP7 in invasion ability. Methods: The present study was carried out to construct C. albicans sap7Δ/Δ mutant strain using a PCR-based gene disruption method. The behaviors of this SAP7 knockout strain was evaluated and compared with the wild type and SAP7 complemented strains between human oral epithelial cells with respect to endocytosis, invasion, and tissue damage. Results: Compared with the wild type C. albicans strain, a 52% reduction in the endocytosis of the sap7Δ/Δ mutant strain by oral epithelial cells was observed, as well as a 25% attenuation of internalization, and a 27% reduction of tissue damage (P<0.05). Conclusion: Our data clearly demonstrates that C. albicans SAP7 contributes to tissue invasion into human oral epithelial cells which warrant further investigations as potential targets for antifungal interventions.
Persistent Identifierhttp://hdl.handle.net/10722/304206
ISSN

 

DC FieldValueLanguage
dc.contributor.authorYang, HP-
dc.contributor.authorTsang, PCS-
dc.contributor.authorTsang, PCS-
dc.contributor.authorPow, EHN-
dc.contributor.authorLam, OLT-
dc.contributor.authorTsang, PWK-
dc.date.accessioned2021-09-23T08:56:43Z-
dc.date.available2021-09-23T08:56:43Z-
dc.date.issued2021-
dc.identifier.citationJournal of Bacteriology and Mycology, 2021, v. 8 n. 5-
dc.identifier.issn2471-0172-
dc.identifier.urihttp://hdl.handle.net/10722/304206-
dc.description.abstractAims: Candida albicans is an important human fungal pathogen in clinical settings. It possesses a wide spectrum of virulence traits, including but not limited to the production of Secreted Aspartic Proteases (SAPs), to invade host cells under predisposing conditions. The aims of the present study were to investigate the functional role of C. albicans SAP7 in invasion ability. Methods: The present study was carried out to construct C. albicans sap7Δ/Δ mutant strain using a PCR-based gene disruption method. The behaviors of this SAP7 knockout strain was evaluated and compared with the wild type and SAP7 complemented strains between human oral epithelial cells with respect to endocytosis, invasion, and tissue damage. Results: Compared with the wild type C. albicans strain, a 52% reduction in the endocytosis of the sap7Δ/Δ mutant strain by oral epithelial cells was observed, as well as a 25% attenuation of internalization, and a 27% reduction of tissue damage (P<0.05). Conclusion: Our data clearly demonstrates that C. albicans SAP7 contributes to tissue invasion into human oral epithelial cells which warrant further investigations as potential targets for antifungal interventions.-
dc.languageeng-
dc.publisherAustin Publishers.-
dc.relation.ispartofJournal of Bacteriology and Mycology-
dc.subjectCandida albicans-
dc.subjectSecreted aspartic protease-
dc.subjectOral epithelial cells-
dc.subjectEndocytosis-
dc.subjectTissue damage-
dc.titleCandida albicans Secreted Aspartic Protease 7 is Essential for Damage of Human Oral Epithelial Cells-
dc.typeArticle-
dc.identifier.emailTsang, PCS: csptsang@hku.hk-
dc.identifier.emailTsang, PCS: csptsang@hku.hk-
dc.identifier.emailPow, EHN: ehnpow@hku.hk-
dc.identifier.authorityTsang, PCS=rp00026-
dc.identifier.authorityTsang, PCS=rp00026-
dc.identifier.authorityPow, EHN=rp00030-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros324918-
dc.identifier.volume8-
dc.identifier.issue5-
dc.publisher.placeUnited States-

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