2009
DOI: 10.1902/jop.2009.090198
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The Role of Toll‐Like Receptor 2 in the Recognition of Aggregatibacter actinomycetemcomitans

Abstract: The results of this study highlight the involvement of TLR2 in recognizing A. actinomycetemcomitans and its essential role in controlling A. actinomycetemcomitans infection.

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Cited by 43 publications
(41 citation statements)
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“…A greater stimulation of TLR4, for example, could enhance the deleterious effects of bacterial LPS, leading to a greater progression of the periapical lesions. Some studies, especially in periodontics, corroborate this hypothesis because increased severity of periodontitis after Aggregatibacter actinomycetemcomitans infection has been observed in TLR2 KO mice (32).…”
Section: Discussionmentioning
confidence: 84%
“…A greater stimulation of TLR4, for example, could enhance the deleterious effects of bacterial LPS, leading to a greater progression of the periapical lesions. Some studies, especially in periodontics, corroborate this hypothesis because increased severity of periodontitis after Aggregatibacter actinomycetemcomitans infection has been observed in TLR2 KO mice (32).…”
Section: Discussionmentioning
confidence: 84%
“…On the other hand, prophylaxis of patients with antibiotics directed mainly against Gram-negative bacteria was not a significant predictive factor in our study even in univariate analysis. Alternatively, there is preliminary evidence that TLR2 is also triggered by certain Gram-negative bacteria [29,30]. In previous studies increasing numbers of GT repeats in intron 2 of the TLR2 gene reduced PamCys and P. acnes-induced TNF, IL6 and IL12 production [16], and the SNP TLR2 Arg753Gln in exon3 was associated with reduced production of TNF and IFN in response to Borrelia burgdorferi [31].…”
Section: Discussionmentioning
confidence: 97%
“…Several host factors, including interferon gamma (22), Toll-like receptor 4 (24), myeloid differentiation primary-response protein 88 (17), p55 tumor necrosis factor alpha (TNF-␣) receptor (21), chemokine receptors CCR1/5 (25,26), macrophage migration inhibitory factor (15), platelet-activator factor receptor (18), and sphingosine kinase 1 (19), have been found to contribute to A. actinomycetemcomitans-induced periodontitis in mice. In contrast, Toll-like receptor 2 has been reported to be important for controlling A. actinomycetemcomitans infection (36), and the antimicrobial agent lactoferrin has been reported to inhibit A. actinomycetemcomitans-induced osteoclastogenesis (27). Interleukin-1 (IL-1) receptor antagonist, which binds to IL-1 receptors, inhibiting IL-1 activity, seems to play a protective role in periodontal disease (28).…”
Section: Figmentioning
confidence: 99%