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Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection

Marina Sabaté Brescó, Llinos Harris Orcid Logo, Keith Thompson, Barbara Stanic, Mario Morgenstern, Liam O'Mahony, R. Geoff Richards, T. Fintan Moriarty

Frontiers in Microbiology, Volume: 8

Swansea University Author: Llinos Harris Orcid Logo

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DOI (Published version): 10.3389/fmicb.2017.01401

Abstract

Staphylococcus epidermidis is a permanent member of the normal human microbiota, commonly found on skin and mucous membranes. By adhering to tissue surface moieties of the host via specific adhesins, S. epidermidis is capable of establishing a lifelong commensal relationship with humans that begins...

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Published in: Frontiers in Microbiology
ISSN: 1664-302X
Published: 2017
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URI: https://cronfa.swan.ac.uk/Record/cronfa35057
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In its role as a commensal organism, S. epidermidis is thought to provide benefits to human host, including out-competing more virulent pathogens. However, largely due to its capacity to form biofilm on implanted foreign bodies, S. epidermidis has emerged as an important opportunistic pathogen in patients receiving medical devices. S. epidermidis causes approximately 20% of all orthopedic device-related infections (ODRIs), increasing up to 50%in late-developing infections. Despite this prevalence, it remains underrepresented in the scientific literature, in particular lagging behind the study of the S. aureus. This review aims to provide an overview of the interactions of S. epidermidis with the human host, both as a commensal and as a pathogen. The mechanisms retained by S. epidermidis that enable colonization of human skin as well as invasive infection, will be described, with a particular focus upon biofilm formation. The host immune responses to these infections are also described, including how S. epidermidis seems to trigger low levels of pro-inflammatory cytokines and high levels of interleukin-10, which may contribute to the sub-acute and persistent nature often associated with these infections. 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spelling 2017-10-31T11:35:08.9851714 v2 35057 2017-08-30 Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection dc70f9d4badbbdb5d467fd321986d173 0000-0002-0295-3038 Llinos Harris Llinos Harris true false 2017-08-30 MEDS Staphylococcus epidermidis is a permanent member of the normal human microbiota, commonly found on skin and mucous membranes. By adhering to tissue surface moieties of the host via specific adhesins, S. epidermidis is capable of establishing a lifelong commensal relationship with humans that begins early in life. In its role as a commensal organism, S. epidermidis is thought to provide benefits to human host, including out-competing more virulent pathogens. However, largely due to its capacity to form biofilm on implanted foreign bodies, S. epidermidis has emerged as an important opportunistic pathogen in patients receiving medical devices. S. epidermidis causes approximately 20% of all orthopedic device-related infections (ODRIs), increasing up to 50%in late-developing infections. Despite this prevalence, it remains underrepresented in the scientific literature, in particular lagging behind the study of the S. aureus. This review aims to provide an overview of the interactions of S. epidermidis with the human host, both as a commensal and as a pathogen. The mechanisms retained by S. epidermidis that enable colonization of human skin as well as invasive infection, will be described, with a particular focus upon biofilm formation. The host immune responses to these infections are also described, including how S. epidermidis seems to trigger low levels of pro-inflammatory cytokines and high levels of interleukin-10, which may contribute to the sub-acute and persistent nature often associated with these infections. The adaptive immune response to S. epidermidis remains poorly described, and represents an area which may provide significant new discoveries in the coming years. Journal Article Frontiers in Microbiology 8 1664-302X Staphylococcus epidermidis; coagulase-negative staphylococci; commensal bacteria; device-related infection; bone infection; immune responses 2 8 2017 2017-08-02 10.3389/fmicb.2017.01401 http://journal.frontiersin.org/article/10.3389/fmicb.2017.01401/full COLLEGE NANME Medical School COLLEGE CODE MEDS Swansea University 2017-10-31T11:35:08.9851714 2017-08-30T10:49:15.5447444 Faculty of Medicine, Health and Life Sciences Swansea University Medical School - Medicine Marina Sabaté Brescó 1 Llinos Harris 0000-0002-0295-3038 2 Keith Thompson 3 Barbara Stanic 4 Mario Morgenstern 5 Liam O'Mahony 6 R. Geoff Richards 7 T. Fintan Moriarty 8 0035057-07092017095035.docx SabateBresco-Review-Frontiers.docx 2017-09-07T09:50:35.8870000 Output 1187615 application/vnd.openxmlformats-officedocument.wordprocessingml.document Accepted Manuscript true 2017-09-07T00:00:00.0000000 true eng 0035057-28092017102027.pdf 35057.pdf 2017-09-28T10:20:27.4170000 Output 2496584 application/pdf Version of Record true 2017-09-28T00:00:00.0000000 This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). true eng
title Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
spellingShingle Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
Llinos Harris
title_short Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
title_full Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
title_fullStr Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
title_full_unstemmed Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
title_sort Pathogenic Mechanisms and Host Interactions in Staphylococcus epidermidis Device-Related Infection
author_id_str_mv dc70f9d4badbbdb5d467fd321986d173
author_id_fullname_str_mv dc70f9d4badbbdb5d467fd321986d173_***_Llinos Harris
author Llinos Harris
author2 Marina Sabaté Brescó
Llinos Harris
Keith Thompson
Barbara Stanic
Mario Morgenstern
Liam O'Mahony
R. Geoff Richards
T. Fintan Moriarty
format Journal article
container_title Frontiers in Microbiology
container_volume 8
publishDate 2017
institution Swansea University
issn 1664-302X
doi_str_mv 10.3389/fmicb.2017.01401
college_str Faculty of Medicine, Health and Life Sciences
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hierarchy_top_id facultyofmedicinehealthandlifesciences
hierarchy_top_title Faculty of Medicine, Health and Life Sciences
hierarchy_parent_id facultyofmedicinehealthandlifesciences
hierarchy_parent_title Faculty of Medicine, Health and Life Sciences
department_str Swansea University Medical School - Medicine{{{_:::_}}}Faculty of Medicine, Health and Life Sciences{{{_:::_}}}Swansea University Medical School - Medicine
url http://journal.frontiersin.org/article/10.3389/fmicb.2017.01401/full
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description Staphylococcus epidermidis is a permanent member of the normal human microbiota, commonly found on skin and mucous membranes. By adhering to tissue surface moieties of the host via specific adhesins, S. epidermidis is capable of establishing a lifelong commensal relationship with humans that begins early in life. In its role as a commensal organism, S. epidermidis is thought to provide benefits to human host, including out-competing more virulent pathogens. However, largely due to its capacity to form biofilm on implanted foreign bodies, S. epidermidis has emerged as an important opportunistic pathogen in patients receiving medical devices. S. epidermidis causes approximately 20% of all orthopedic device-related infections (ODRIs), increasing up to 50%in late-developing infections. Despite this prevalence, it remains underrepresented in the scientific literature, in particular lagging behind the study of the S. aureus. This review aims to provide an overview of the interactions of S. epidermidis with the human host, both as a commensal and as a pathogen. The mechanisms retained by S. epidermidis that enable colonization of human skin as well as invasive infection, will be described, with a particular focus upon biofilm formation. The host immune responses to these infections are also described, including how S. epidermidis seems to trigger low levels of pro-inflammatory cytokines and high levels of interleukin-10, which may contribute to the sub-acute and persistent nature often associated with these infections. The adaptive immune response to S. epidermidis remains poorly described, and represents an area which may provide significant new discoveries in the coming years.
published_date 2017-08-02T19:11:21Z
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