Host cell invasion and virulence mediated by Candida albicans Ssa1.

Candida albicans Ssa1 and Ssa2 are members of the HSP70 family of heat shock proteins that are expressed on the cell surface and function as receptors for antimicrobial peptides such as histatins. We investigated the role of Ssa1 and Ssa2 in mediating pathogenic host cell interactions and virulence....

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Main Authors: Jianing N Sun, Norma V Solis, Quynh T Phan, Jashanjot S Bajwa, Helena Kashleva, Angela Thompson, Yaoping Liu, Anna Dongari-Bagtzoglou, Mira Edgerton, Scott G Filler
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2010-11-01
Series:PLoS Pathogens
Online Access:https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1001181&type=printable
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author Jianing N Sun
Norma V Solis
Quynh T Phan
Jashanjot S Bajwa
Helena Kashleva
Angela Thompson
Yaoping Liu
Anna Dongari-Bagtzoglou
Mira Edgerton
Scott G Filler
author_facet Jianing N Sun
Norma V Solis
Quynh T Phan
Jashanjot S Bajwa
Helena Kashleva
Angela Thompson
Yaoping Liu
Anna Dongari-Bagtzoglou
Mira Edgerton
Scott G Filler
author_sort Jianing N Sun
collection DOAJ
description Candida albicans Ssa1 and Ssa2 are members of the HSP70 family of heat shock proteins that are expressed on the cell surface and function as receptors for antimicrobial peptides such as histatins. We investigated the role of Ssa1 and Ssa2 in mediating pathogenic host cell interactions and virulence. A C. albicans ssa1Δ/Δ mutant had attenuated virulence in murine models of disseminated and oropharyngeal candidiasis, whereas an ssa2Δ/Δ mutant did not. In vitro studies revealed that the ssa1Δ/Δ mutant caused markedly less damage to endothelial cells and oral epithelial cell lines. Also, the ssa1Δ/Δ mutant had defective binding to endothelial cell N-cadherin and epithelial cell E-cadherin, receptors that mediate host cell endocytosis of C. albicans. As a result, this mutant had impaired capacity to induce its own endocytosis by endothelial cells and oral epithelial cells. Latex beads coated with recombinant Ssa1 were avidly endocytosed by both endothelial cells and oral epithelial cells, demonstrating that Ssa1 is sufficient to induce host cell endocytosis. These results indicate that Ssa1 is a novel invasin that binds to host cell cadherins, induces host cell endocytosis, and is critical for C. albicans to cause maximal damage to host cells and induce disseminated and oropharyngeal disease.
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spelling doaj-art-ac9894ee30824f00a6fcd382cef88be32025-08-20T03:07:21ZengPublic Library of Science (PLoS)PLoS Pathogens1553-73661553-73742010-11-01611e100118110.1371/journal.ppat.1001181Host cell invasion and virulence mediated by Candida albicans Ssa1.Jianing N SunNorma V SolisQuynh T PhanJashanjot S BajwaHelena KashlevaAngela ThompsonYaoping LiuAnna Dongari-BagtzoglouMira EdgertonScott G FillerCandida albicans Ssa1 and Ssa2 are members of the HSP70 family of heat shock proteins that are expressed on the cell surface and function as receptors for antimicrobial peptides such as histatins. We investigated the role of Ssa1 and Ssa2 in mediating pathogenic host cell interactions and virulence. A C. albicans ssa1Δ/Δ mutant had attenuated virulence in murine models of disseminated and oropharyngeal candidiasis, whereas an ssa2Δ/Δ mutant did not. In vitro studies revealed that the ssa1Δ/Δ mutant caused markedly less damage to endothelial cells and oral epithelial cell lines. Also, the ssa1Δ/Δ mutant had defective binding to endothelial cell N-cadherin and epithelial cell E-cadherin, receptors that mediate host cell endocytosis of C. albicans. As a result, this mutant had impaired capacity to induce its own endocytosis by endothelial cells and oral epithelial cells. Latex beads coated with recombinant Ssa1 were avidly endocytosed by both endothelial cells and oral epithelial cells, demonstrating that Ssa1 is sufficient to induce host cell endocytosis. These results indicate that Ssa1 is a novel invasin that binds to host cell cadherins, induces host cell endocytosis, and is critical for C. albicans to cause maximal damage to host cells and induce disseminated and oropharyngeal disease.https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1001181&type=printable
spellingShingle Jianing N Sun
Norma V Solis
Quynh T Phan
Jashanjot S Bajwa
Helena Kashleva
Angela Thompson
Yaoping Liu
Anna Dongari-Bagtzoglou
Mira Edgerton
Scott G Filler
Host cell invasion and virulence mediated by Candida albicans Ssa1.
PLoS Pathogens
title Host cell invasion and virulence mediated by Candida albicans Ssa1.
title_full Host cell invasion and virulence mediated by Candida albicans Ssa1.
title_fullStr Host cell invasion and virulence mediated by Candida albicans Ssa1.
title_full_unstemmed Host cell invasion and virulence mediated by Candida albicans Ssa1.
title_short Host cell invasion and virulence mediated by Candida albicans Ssa1.
title_sort host cell invasion and virulence mediated by candida albicans ssa1
url https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1001181&type=printable
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