TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia

T. Strunk; M.R. Power Coombs; A.J. Currie; P. Richmond; D.T. Golenbock; L. Stoler-Barak; L.C. Gallington; M. Otto; D. Burgner; O. Levy

doi:10.1371/journal.pone.0010111

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TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia

Journal article

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TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia

T. Strunk, M.R. Power Coombs, A.J. Currie, P. Richmond, D.T. Golenbock, L. Stoler-Barak, L.C. Gallington, M. Otto, D. Burgner and O. Levy

PLoS ONE, Vol.5(4), e10111

2010

DOI: https://doi.org/10.1371/journal.pone.0010111

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Abstract

Background: Staphylococcus epidermidis (SE) is a nosocomial pathogen that causes catheter-associated bacteremia in the immunocompromised, including those at the extremes of age, motivating study of host clearance mechanisms. SE-derived soluble components engage TLR2; but additional signaling pathways have also been implicated, and TLR2 can play complex, at times detrimental, roles in host defense against other Staphylococcal spp. The role of TLR2 in responses of primary blood leukocytes to live SE and in clearance of SE bacteremia, the most common clinical manifestation of SE infection, is unknown. Methodology/Principal Findings: We studied TLR2-mediated recognition of live clinical SE strain 1457 employing TLR2- transfected cells, neutralizing anti-TLR antibodies and TLR2-deficient mice. TLR2 mediated SE-induced cytokine production in human embryonic kidney cells, human whole blood and murine primary macrophages, in part via recognition of a soluble TLR2 agonist. After i.v. challenge with SE, early (1 h) cytokine/chemokine production and subsequent clearance of bacteremia (24-48 h) were markedly impaired in TLR2-deficient mice. Conclusions/Significance: TLR2 mediates recognition of live SE and clearance of SE bacteremia in vivo.

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Title: TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia
Authors/Creators: T. Strunk (Author/Creator) - The University of Western Australia
M.R. Power Coombs (Author/Creator)
A.J. Currie (Author/Creator) - The University of Western Australia
P. Richmond (Author/Creator) - The University of Western Australia
D.T. Golenbock (Author/Creator) - University of Massachusetts Chan Medical School
L. Stoler-Barak (Author/Creator) - Boston Children's Hospital
L.C. Gallington (Author/Creator) - Boston Children's Hospital
M. Otto (Author/Creator) - National Institute of Allergy and Infectious Diseases
D. Burgner (Author/Creator) - Royal Children's Hospital
O. Levy (Author/Creator) - Boston Children's Hospital
Publication Details: PLoS ONE, Vol.5(4), e10111
Publisher: Public Library of Science
Identifiers: 991005540984507891
Copyright: This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or ot
Murdoch Affiliation: Murdoch University
Language: English
Resource Type: Journal article

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Collaboration types: Domestic collaboration; International collaboration
Citation topics: 1 Clinical & Life Sciences; 1.6 Immunology; 1.6.609 Toll-like Receptors
Web Of Science research areas: Immunology
ESI research areas: Immunology