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Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model

Candida albicans is an opportunistic pathogen found throughout multiple body sites and is frequently co-isolated from infections of the respiratory tract and oral cavity with Staphylococcus aureus. Herein we present the first report of the effects that S. aureus elicits on the C. albicans transcript...

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Autores principales: Short, Bryn, Delaney, Christopher, McKloud, Emily, Brown, Jason L., Kean, Ryan, Litherland, Gary J., Williams, Craig, Martin, S. Lorraine, MacKay, William G., Ramage, Gordon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8650683/
https://www.ncbi.nlm.nih.gov/pubmed/34888261
http://dx.doi.org/10.3389/fcimb.2021.791523
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author Short, Bryn
Delaney, Christopher
McKloud, Emily
Brown, Jason L.
Kean, Ryan
Litherland, Gary J.
Williams, Craig
Martin, S. Lorraine
MacKay, William G.
Ramage, Gordon
author_facet Short, Bryn
Delaney, Christopher
McKloud, Emily
Brown, Jason L.
Kean, Ryan
Litherland, Gary J.
Williams, Craig
Martin, S. Lorraine
MacKay, William G.
Ramage, Gordon
author_sort Short, Bryn
collection PubMed
description Candida albicans is an opportunistic pathogen found throughout multiple body sites and is frequently co-isolated from infections of the respiratory tract and oral cavity with Staphylococcus aureus. Herein we present the first report of the effects that S. aureus elicits on the C. albicans transcriptome. Dual-species biofilms containing S. aureus and C. albicans mutants defective in ALS3 or ECE1 were optimised and characterised, followed by transcriptional profiling of C. albicans by RNA-sequencing (RNA-seq). Altered phenotypes in C. albicans mutants revealed specific interaction profiles between fungus and bacteria. The major adhesion and virulence proteins Als3 and Ece1, respectively, were found to have substantial effects on the Candida transcriptome in early and mature biofilms. Despite this, deletion of ECE1 did not adversely affect biofilm formation or the ability of S. aureus to interact with C. albicans hyphae. Upregulated genes in dual-species biofilms corresponded to multiple gene ontology terms, including those attributed to virulence, biofilm formation and protein binding such as ACE2 and multiple heat-shock protein genes. This shows that S. aureus pushes C. albicans towards a more virulent genotype, helping us to understand the driving forces behind the increased severity of C. albicans-S. aureus infections.
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spelling pubmed-86506832021-12-08 Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model Short, Bryn Delaney, Christopher McKloud, Emily Brown, Jason L. Kean, Ryan Litherland, Gary J. Williams, Craig Martin, S. Lorraine MacKay, William G. Ramage, Gordon Front Cell Infect Microbiol Cellular and Infection Microbiology Candida albicans is an opportunistic pathogen found throughout multiple body sites and is frequently co-isolated from infections of the respiratory tract and oral cavity with Staphylococcus aureus. Herein we present the first report of the effects that S. aureus elicits on the C. albicans transcriptome. Dual-species biofilms containing S. aureus and C. albicans mutants defective in ALS3 or ECE1 were optimised and characterised, followed by transcriptional profiling of C. albicans by RNA-sequencing (RNA-seq). Altered phenotypes in C. albicans mutants revealed specific interaction profiles between fungus and bacteria. The major adhesion and virulence proteins Als3 and Ece1, respectively, were found to have substantial effects on the Candida transcriptome in early and mature biofilms. Despite this, deletion of ECE1 did not adversely affect biofilm formation or the ability of S. aureus to interact with C. albicans hyphae. Upregulated genes in dual-species biofilms corresponded to multiple gene ontology terms, including those attributed to virulence, biofilm formation and protein binding such as ACE2 and multiple heat-shock protein genes. This shows that S. aureus pushes C. albicans towards a more virulent genotype, helping us to understand the driving forces behind the increased severity of C. albicans-S. aureus infections. Frontiers Media S.A. 2021-11-23 /pmc/articles/PMC8650683/ /pubmed/34888261 http://dx.doi.org/10.3389/fcimb.2021.791523 Text en Copyright © 2021 Short, Delaney, McKloud, Brown, Kean, Litherland, Williams, Martin, MacKay and Ramage https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cellular and Infection Microbiology
Short, Bryn
Delaney, Christopher
McKloud, Emily
Brown, Jason L.
Kean, Ryan
Litherland, Gary J.
Williams, Craig
Martin, S. Lorraine
MacKay, William G.
Ramage, Gordon
Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title_full Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title_fullStr Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title_full_unstemmed Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title_short Investigating the Transcriptome of Candida albicans in a Dual-Species Staphylococcus aureus Biofilm Model
title_sort investigating the transcriptome of candida albicans in a dual-species staphylococcus aureus biofilm model
topic Cellular and Infection Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8650683/
https://www.ncbi.nlm.nih.gov/pubmed/34888261
http://dx.doi.org/10.3389/fcimb.2021.791523
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