Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus
Abstract Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis. These infections are notoriously difficult to treat, and it is believed that the ability of S. aureus to invade endothelial cells and persist intracellularly is a key mechanism for persistence...
Príomhchruthaitheoirí: | , , , , , , , |
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Formáid: | Alt |
Teanga: | English |
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Nature Portfolio
2021-03-01
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Sraith: | Scientific Reports |
Rochtain ar líne: | https://doi.org/10.1038/s41598-021-84050-x |
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author | Rasmus Birkholm Grønnemose Christian Garde Claes Søndergaard Wassmann Janne Kudsk Klitgaard Ronni Nielsen Susanne Mandrup Andreas Holm Mattsson Thomas Emil Andersen |
author_facet | Rasmus Birkholm Grønnemose Christian Garde Claes Søndergaard Wassmann Janne Kudsk Klitgaard Ronni Nielsen Susanne Mandrup Andreas Holm Mattsson Thomas Emil Andersen |
author_sort | Rasmus Birkholm Grønnemose |
collection | DOAJ |
description | Abstract Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis. These infections are notoriously difficult to treat, and it is believed that the ability of S. aureus to invade endothelial cells and persist intracellularly is a key mechanism for persistence despite ongoing antibiotic treatment. Here, we used dual RNA sequencing to study the simultaneous transcriptional response of S. aureus and human endothelial cells during in vitro infections. We revealed discrete and shared differentially expressed genes for both host and pathogen at the different stages of infection. While the endothelial cells upregulated genes involved in interferon signalling and antigen presentation during late infection, S. aureus downregulated toxin expression while upregulating genes related to iron scavenging. In conclusion, the presented data provide an important resource to facilitate functional investigations into host–pathogen interaction during S. aureus invasive infection and a basis for identifying novel drug target sites. |
first_indexed | 2024-12-17T11:11:41Z |
format | Article |
id | doaj.art-ebcbb48b41e24b86a95acf5c2d1df2bc |
institution | Directory Open Access Journal |
issn | 2045-2322 |
language | English |
last_indexed | 2024-12-17T11:11:41Z |
publishDate | 2021-03-01 |
publisher | Nature Portfolio |
record_format | Article |
series | Scientific Reports |
spelling | doaj.art-ebcbb48b41e24b86a95acf5c2d1df2bc2022-12-21T21:51:26ZengNature PortfolioScientific Reports2045-23222021-03-0111111110.1038/s41598-021-84050-xBacteria-host transcriptional response during endothelial invasion by Staphylococcus aureusRasmus Birkholm Grønnemose0Christian Garde1Claes Søndergaard Wassmann2Janne Kudsk Klitgaard3Ronni Nielsen4Susanne Mandrup5Andreas Holm Mattsson6Thomas Emil Andersen7Research Unit of Clinical Microbiology, University of Southern Denmark and Odense University HospitalEvaxion Biotech A/SResearch Unit of Molecular Microbiology, Department of Biochemistry and Molecular Biology, University of Southern DenmarkResearch Unit of Clinical Microbiology, University of Southern Denmark and Odense University HospitalFunctional Genomics and Metabolism Research Unit, Department of Biochemistry and Molecular Biology, University of Southern DenmarkFunctional Genomics and Metabolism Research Unit, Department of Biochemistry and Molecular Biology, University of Southern DenmarkEvaxion Biotech A/SResearch Unit of Clinical Microbiology, University of Southern Denmark and Odense University HospitalAbstract Staphylococcus aureus is the cause of serious vascular infections such as sepsis and endocarditis. These infections are notoriously difficult to treat, and it is believed that the ability of S. aureus to invade endothelial cells and persist intracellularly is a key mechanism for persistence despite ongoing antibiotic treatment. Here, we used dual RNA sequencing to study the simultaneous transcriptional response of S. aureus and human endothelial cells during in vitro infections. We revealed discrete and shared differentially expressed genes for both host and pathogen at the different stages of infection. While the endothelial cells upregulated genes involved in interferon signalling and antigen presentation during late infection, S. aureus downregulated toxin expression while upregulating genes related to iron scavenging. In conclusion, the presented data provide an important resource to facilitate functional investigations into host–pathogen interaction during S. aureus invasive infection and a basis for identifying novel drug target sites.https://doi.org/10.1038/s41598-021-84050-x |
spellingShingle | Rasmus Birkholm Grønnemose Christian Garde Claes Søndergaard Wassmann Janne Kudsk Klitgaard Ronni Nielsen Susanne Mandrup Andreas Holm Mattsson Thomas Emil Andersen Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus Scientific Reports |
title | Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus |
title_full | Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus |
title_fullStr | Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus |
title_full_unstemmed | Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus |
title_short | Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus |
title_sort | bacteria host transcriptional response during endothelial invasion by staphylococcus aureus |
url | https://doi.org/10.1038/s41598-021-84050-x |
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