Toll-like receptor 2 (TLR2) has been associated with mechanical-stress-mediated activation of signalling pathways that may lead to inflammation, apoptosis, and atherosclerosis.
Further analysis revealed that RYR might attenuate atherosclerosis through inhibiting hydroxy methylglutaryl-CoA reductase and the consequent inflammatory signaling pathways mediated by TLR2 and TLR4.
TRL2 and TLR4 were dispensable for systemic spread after polybacterial infections but TLR2 and 4 deficiency markedly reduces atherosclerosis induced by oral bacteria.
Although infection with periodontal and respiratory pathogens via activation of inflammatory cell Toll-like receptor (TLR)2 has been linked to vascular disease, little is known about smooth muscle cell TLR2 in atherosclerosis.
We evaluated the role of TLR2 and TLR4 signaling in the induction of both PD and atherosclerosis in TLR2<sup>-/-</sup> and TLR4<sup>-/-</sup> mice to polymicrobial infection with periodontal pathogens Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum.
These results suggest that commensal Bacteriodetes bacteria of the gut and the oral cavity may contribute to the pathogenesis of TLR2-dependent atherosclerosis through serine dipeptide lipid deposition and metabolism in artery walls.
We hypothesize that up-regulation of TLR2 by intermittent hypoxia may lead to systemic inflammation, insulin resistance and atherosclerosis in patients with obstructive sleep apnea.
We suggest that VB-201 may counter inflammation where TLR-2 and/or CD14 complicity is essential, and is therefore beneficial for the treatment of atherosclerosis.
We show in vitro data on the potential role of high glucose in increasing LPS-induced TLR2 expression and inflammatory cytokine secretion in HUVECs, offering a new insight into the pathophysiological pathways involved in atherosclerosis.
These observations are mitigated by CPAP therapy, which suggest that TLR2 and TLR4 activation may be involved as a signaling mechanism in immune-mediated progression of atherosclerosis in OSA.
The aim of the study was to assess the frequency of SNP896A/G in the Toll-like receptor (TLR) 4 gene and SNP1350T/C in the TLR2 gene in patients with acute myocardial infarction (AMI) and to analyse the association of these SNPs with risk factors for atherosclerosis and clinical aspects of AMI in a sample of the Croatian population.
Examples include variants of TLR4 in sepsis, malaria, inflammatory bowel disease and atherosclerosis; variants in TLR2 in tuberculosis and asthma; a variant in Mal (a key signal for TLR2 and TLR4) in malaria, tuberculosis and systemic lupus erythematosus; and variants in the kinase IRAK4 in pyogenic infections.
TLR-2 is a key innate immunity receptor for sensing both endogenous inflammatory mediators and ligands of several microbial pathogens postulated to be involved in atherosclerosis.