Linked Life Data

21525381

Source:http://linkedlifedata.com/resource/pubmed/id/21525381

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2011-5-20
pubmed:abstractText
Biofilms are complex communities of bacteria encased in a matrix composed primarily of polysaccharides, extracellular DNA, and protein. Staphylococcus aureus can form biofilm infections, which are often debilitating due to their chronicity and recalcitrance to antibiotic therapy. Currently, the immune mechanisms elicited during biofilm growth and their impact on bacterial clearance remain to be defined. We used a mouse model of catheter-associated biofilm infection to assess the functional importance of TLR2 and TLR9 in the host immune response during biofilm formation, because ligands for both receptors are present within the biofilm. Interestingly, neither TLR2 nor TLR9 impacted bacterial density or inflammatory mediator secretion during biofilm growth in vivo, suggesting that S. aureus biofilms circumvent these traditional bacterial recognition pathways. Several potential mechanisms were identified to account for biofilm evasion of innate immunity, including significant reductions in IL-1?, TNF-?, CXCL2, and CCL2 expression during biofilm infection compared with the wound healing response elicited by sterile catheters, limited macrophage invasion into biofilms in vivo, and a skewing of the immune response away from a microbicidal phenotype as evidenced by decreases in inducible NO synthase expression concomitant with robust arginase-1 induction. Coculture studies of macrophages with S. aureus biofilms in vitro revealed that macrophages successful at biofilm invasion displayed limited phagocytosis and gene expression patterns reminiscent of alternatively activated M2 macrophages. Collectively, these findings demonstrate that S. aureus biofilms are capable of attenuating traditional host proinflammatory responses, which may explain why biofilm infections persist in an immunocompetent host.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6585-96
pubmed:dateRevised
2011-9-26
pubmed:meshHeading
pubmed-meshheading:21525381-Animals, pubmed-meshheading:21525381-Biofilms, pubmed-meshheading:21525381-Catheter-Related Infections, pubmed-meshheading:21525381-Cytokines, pubmed-meshheading:21525381-Green Fluorescent Proteins, pubmed-meshheading:21525381-Host-Pathogen Interactions, pubmed-meshheading:21525381-Immune Evasion, pubmed-meshheading:21525381-Inflammation, pubmed-meshheading:21525381-Macrophages, pubmed-meshheading:21525381-Mice, pubmed-meshheading:21525381-Mice, Inbred C57BL, pubmed-meshheading:21525381-Mice, Knockout, pubmed-meshheading:21525381-Mice, Transgenic, pubmed-meshheading:21525381-Microscopy, Confocal, pubmed-meshheading:21525381-Microscopy, Electron, Scanning, pubmed-meshheading:21525381-Models, Immunological, pubmed-meshheading:21525381-Phagocytosis, pubmed-meshheading:21525381-Staphylococcal Infections, pubmed-meshheading:21525381-Staphylococcus aureus, pubmed-meshheading:21525381-Toll-Like Receptor 2, pubmed-meshheading:21525381-Toll-Like Receptor 9
pubmed:year
2011
pubmed:articleTitle
Staphylococcus aureus biofilms prevent macrophage phagocytosis and attenuate inflammation in vivo.
pubmed:affiliation
Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural