TLR2 mediates recognition of live Staphylococcus epidermidis and clearance of bacteremia
Power Coombs, Melanie R.
Currie, Andrew J.
Golenbock, Douglas T.
Gallington, Leighanne C.
UMass Chan AffiliationsDepartment of Medicine, Division of Infectious Diseases and Immunology
Document TypeJournal Article
Immunology and Infectious Disease
Immunology of Infectious Disease
MetadataShow full item record
AbstractBACKGROUND: 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.
PLoS One. 2010 Apr 9;5(4):e10111. doi: 10.1371/journal.pone.0010111. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/35167
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by/4.0/