TY - JOUR
T1 - Functional TLRs and NODs in human gingival fibroblasts
AU - Uehara, A.
AU - Takada, H.
N1 - Funding Information:
We thank D. Mrozek (Medical English Service, Kyoto, Japan) for organizing the review of this paper. This study was supported by a Grant-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (18390484) and by the Naito Memorial Foundation (to A.U.).
PY - 2007/3
Y1 - 2007/3
N2 - Since human gingival fibroblasts are the major cells in periodontal tissues, we hypothesized that gingival fibroblasts are endowed with receptors for bacterial components, which induce innate immune responses against invading bacteria. We found clear mRNA expression of Toll-like receptors (TLR)1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, MD-2, MyD88, NOD1, and NOD2 in gingival fibroblasts. Gingival fibroblasts constitutively expressed these molecules. Upon stimulation with chemically synthesized ligands mimicking microbial products for these receptors, the production of proinflammatory cytokines, such as interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1, was markedly up-regulated. Furthermore, the production of pro-inflammatory cytokines induced by TLR and NOD ligands was significantly inhibited by an RNA interference assay targeted to NF-κB. These findings indicate that these innate immunity-related molecules in gingival fibroblasts are functional receptors involved in inflammatory reactions in periodontal tissues, which might be responsible for periodontal pathogenesis.
AB - Since human gingival fibroblasts are the major cells in periodontal tissues, we hypothesized that gingival fibroblasts are endowed with receptors for bacterial components, which induce innate immune responses against invading bacteria. We found clear mRNA expression of Toll-like receptors (TLR)1, TLR2, TLR3, TLR4, TLR5, TLR6, TLR7, TLR8, TLR9, MD-2, MyD88, NOD1, and NOD2 in gingival fibroblasts. Gingival fibroblasts constitutively expressed these molecules. Upon stimulation with chemically synthesized ligands mimicking microbial products for these receptors, the production of proinflammatory cytokines, such as interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1, was markedly up-regulated. Furthermore, the production of pro-inflammatory cytokines induced by TLR and NOD ligands was significantly inhibited by an RNA interference assay targeted to NF-κB. These findings indicate that these innate immunity-related molecules in gingival fibroblasts are functional receptors involved in inflammatory reactions in periodontal tissues, which might be responsible for periodontal pathogenesis.
KW - Fibroblasts
KW - Innate immunity
KW - NOD1
KW - NOD2
KW - TLR
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U2 - 10.1177/154405910708600310
DO - 10.1177/154405910708600310
M3 - Article
C2 - 17314257
AN - SCOPUS:33947356654
VL - 86
SP - 249
EP - 254
JO - Journal of Dental Research
JF - Journal of Dental Research
SN - 0022-0345
IS - 3
ER -