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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2010-6-18
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pubmed:abstractText |
Studies in humans have established that polymorphisms in genes encoding the innate immune Toll-like receptors (TLRs) are associated with inflammatory atherosclerosis. In hyperlipidemic mice, TLR2 and TLR4 have been reported to contribute to atherosclerosis progression. Human and mouse studies support a role for the oral pathogen Porphyromonas gingivalis in atherosclerosis, although the mechanisms by which this pathogen stimulates inflammatory atherosclerosis via innate immune system activation is not known. Using a genetically defined apolipoprotein E-deficient (ApoE(-/-)) mouse model we demonstrate that pathogen-mediated inflammatory atherosclerosis occurs via both TLR2-dependent and TLR2-independent mechanisms. P. gingivalis infection in mice possessing functional TLR2 induced the accumulation of macrophages as well as inflammatory mediators including CD40, IFN-gamma and the pro-inflammatory cytokines IL-1 beta, IL-6 and tumor necrosis factor-alpha in atherosclerotic lesions. The expression of these inflammatory mediators was reduced in atherosclerotic lesions from P. gingivalis-infected TLR2-deficient (TLR2(-/-)) mice. These studies provide a mechanistic link between an innate immune receptor and pathogen-accelerated atherosclerosis by a clinically and biologically relevant bacterial pathogen.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20505314-10027806,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20505314-10860949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20505314-11705986,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/20505314-9541503
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:issn |
1662-8128
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pubmed:author |
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pubmed:copyrightInfo |
(c) 2010 S. Karger AG, Basel.
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pubmed:issnType |
Electronic
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pubmed:volume |
2
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
334-43
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pubmed:dateRevised |
2011-7-28
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pubmed:meshHeading |
pubmed-meshheading:20505314-Animals,
pubmed-meshheading:20505314-Apolipoproteins E,
pubmed-meshheading:20505314-Atherosclerosis,
pubmed-meshheading:20505314-Bacteroidaceae Infections,
pubmed-meshheading:20505314-Cytokines,
pubmed-meshheading:20505314-Disease Models, Animal,
pubmed-meshheading:20505314-Humans,
pubmed-meshheading:20505314-Inflammation,
pubmed-meshheading:20505314-Inflammation Mediators,
pubmed-meshheading:20505314-Macrophages,
pubmed-meshheading:20505314-Male,
pubmed-meshheading:20505314-Mice,
pubmed-meshheading:20505314-Mice, Inbred C57BL,
pubmed-meshheading:20505314-Porphyromonas gingivalis,
pubmed-meshheading:20505314-Toll-Like Receptor 2
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pubmed:year |
2010
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pubmed:articleTitle |
Pathogen-mediated inflammatory atherosclerosis is mediated in part via Toll-like receptor 2-induced inflammatory responses.
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pubmed:affiliation |
Department of Medicine, Sections of Infectious Diseases, Boston University School of Medicine, Boston, MA 02118, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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