Expression of Toll-like Receptor 2 and 4 in Dental Pulp

Mutoh, Noriko; Tani‐Ishii, Nobuyuki; Tsukinoki, Keiichi; Chieda, Keiko; Watanabe, Koichi

doi:10.1016/j.joen.2007.05.018

Cited by 90 publications

(81 citation statements)

References 18 publications

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“…TLR2 upregulation was observed in vivo in odontoblasts of mouse molar pulps experimentally inflamed with intradentinal Gram-positive bacteria (Mutoh et al, 2007). In this study, we report TLR2 protein expression in pulp of carious human molars (Fig.…”

Section: Recognition Of Bacteria By Odontoblastssupporting

confidence: 57%

Odontoblasts in the dental pulp immune response

et al. 2008

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Recent studies have demonstrated that human dental pulp cells sense pathogens and elicit innate and/or adaptive immunity. Particular attention has been paid to odontoblasts that are situated at the pulp-dentin interface and constitute the first line of defense to cariogenic bacteria entering dentin after enamel disruption. In this review, recent in vitro and in vivo data suggesting that odontoblasts initiate immune/inflammatory events within the dental pulp in response to cariogenic bacteria are discussed. These data include sensing of pathogens by Toll-like receptors (TLRs), production of chemokines upon cell stimulation with microbial by-products and induction of dendritic cell migration. Additional results presented here reveal that all TLR genes are expressed in the healthy human dental pulp that is thus well equipped to combat pathogens entering the tissue. Seventeen chemokine genes including CXCL12, CCL2, CXCL9, CX3CL1, CCL8, CXCL10, CCL16, CCL5, CXCL2, CCL4, CXCL11 and CCL3, and 9 chemokine receptor genes including CXCR4, CCR1, CCR5, CX3CR1, CCR10 and CXCR3, are also expressed in pulp. TLR2, CCL2 and CXCL1 are upregulated in odontoblasts both under caries lesions and upon stimulation with pathogen by-products. These molecules thus appear as preferential targets for the design of therapeutic agents able to reduce the immune/inflammatory response to cariogenic bacteria and favor pulp healing.

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Section: Recognition Of Bacteria By Odontoblastssupporting

confidence: 57%

Odontoblasts in the dental pulp immune response

et al. 2008

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“…Recently, it has been reported that HDPCs express TLR2 and TLR4 and therefore retain the ability to participate in the innate immune response (Mutoh et al, 2007). Similar to TLRs, nucleotide-binding oligomerization domain-containing protein 1 (NOD1) and NOD2 are intracellular patternrecognition receptors, which recognize a specific molecular structure called muramyl dipeptide (MDP) in Gram-positive/negative bacteria (Girardin et al, 2003).…”

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confidence: 99%

NOD2 Mediates Odontoblast Differentiation and RANKL Expression

Lee

Kim

et al. 2014

J Dent Res

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The precise regulation of odontoblast differentiation and osteoclastogenic cytokine expression in human dental pulp cells (HDPCs) is crucial for the pathology of bacteria-related pulpitis. Although the up-regulation of nucleotide-binding oligomerization domain-containing protein 2 (NOD2) has been reported in inflamed human dental pulps, the role of NOD2 in the differentiation of HDPCs remains unclear. Here, we show the involvement of NOD2 in odontoblast differentiation together with osteoclastogenic cytokine expression in HDPCs. Treatment with muramyl dipeptide (MDP), a known NOD2-agonist, significantly inhibited odontoblast differentiation of HDPCs, as revealed by reduced ALP activity, osteoblast/ odontoblast marker expression, and mineralized nodule formation. Importantly, the forced down-regulation of NOD2 by small interfering RNA (siRNA) recovered MDP-down-regulated odontoblast differentiation. MDP-elicited suppression of odontoblast differentiation resulted from the increased expression of MKP-1 protein and the subsequent decline of MAPKs phosphorylation, which is a prerequisite for odontoblast differentiation. Furthermore, we found that MDP treatment elevated the expression of osteoclastogenic cytokines in HDPCs, which was also reversed by NOD2 silencing. Analysis of these data, taken together, suggests that the regulation of NOD2 expression upon MDP challenge might serve as an intrinsic mechanism that underlies the hindered dentin formation and accelerated dentin resorption in bacterial infection-mediated pulpitis.Abbreviations: HDPCs, human dental pulp cells; NOD2, nucleotide-binding oligomerization domain-containing protein 2; MDP, muramyl dipeptide; siRNA, small interfering RNA; MAPKs, mitogen-activated protein kinases; MKP-1, MAPK phosphatase-1; BMMs, bone-marrow-derived macrophages; and CM, conditioned medium.

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“…Odontoblasts express TLR2 and TLR4 on the cellular processes and cell surfaces, suggesting a capacity of odontoblasts to receive signals from Gram-positive and Gram negative bacteria in tooth decay (Figure 1). [19][20][21][22] As mentioned earlier, TLR2 is crucial for the recognition of Gram-positive bacteria components, including LTA, lipopeptides, and peptidoglycan. Meanwhile, TLR4 is the predominant receptor for LPS, a characteristic component of the cell wall of Gram-negative bacteria.…”

Section: 14 Discussionmentioning

confidence: 90%

Potential role of odontoblasts in the innate immune response of the dental pulp

Haniastuti

2008

Dent. J. (Majalah Kedokteran Gigi)

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Expression of Toll-like Receptor 2 and 4 in Dental Pulp

Cited by 90 publications

References 18 publications

Odontoblasts in the dental pulp immune response

Odontoblasts in the dental pulp immune response

NOD2 Mediates Odontoblast Differentiation and RANKL Expression

Potential role of odontoblasts in the innate immune response of the dental pulp

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