Journal
JOURNAL OF INNATE IMMUNITY
Volume 2, Issue 4, Pages 334-343Publisher
KARGER
DOI: 10.1159/000314686
Keywords
Toll-like receptor 2; Inflammation; Porphyromonas gingivalis; Pro-inflammatory cytokines; Atherosclerosis
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Funding
- NIH Public Health Service [HL080387]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL080387] Funding Source: NIH RePORTER
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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 apolipoprotien 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-6 and tumor necrosis factor-a 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. Copyright (C) 2010 S. Karger AG, Basel
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