| Co-Investigator(Kenkyū-buntansha) |
NEMOTO Eiji Tohoku University, Graduate School of Dentistry, Assistant Professor, 大学院・歯学研究科, 助手 (40292221)
TAKADA Haruhiko Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (30135743)
|
|---|
| Research Abstract |
1. Oral epithelial cells constitutively express precursor form of interleukin-18 (IL-18) in the cells. Bioactive IL-18 was produced from the cells on costimulation with neutrophil serine proteinase, proteinase 3 (PR3), and Iipopolysaccharide (LPS) after interferon-γ (IFN-γ)-priming. PR3 was found to activate oral epithelial cells through G protein-coupled protease-activated receptor-2.
2. Oral epithelial cells do not express a bacterial pattern recognition receptor, CD 14, and express Toll-like receptors (TLRs)/MD-2/MyD88 system, which is critical in innate immune recognition. However, the cells are refractory to bacterial components even in the presence of soluble CD14, The cells are able to respond to components from black-pigmented bacteria (BPB). The cells acquire responsiveness to many bacterial components after priming with IFN-γ.
3. Nonendotoxic glycoprotein from BPB activates host cells in a CD14- and TLR2-dependent manner.
4. CD14-expreswsing human gingival fibroblasts (HGF) have the same property with oral epithelial cells. Human periodontal ligament fibroblasts (HPLF) express TLR2 more strongly than HGF. HGF mainly respond to Gram-negative, and HPLF mainly respond to Gram-positive bacterial components, respectively. Cysteine proteinases (gingipains) from periodontopafhic bacteria degrade CD14 on HGF, consequently, suppress CD14-dependent responsiveness to bacterial components.
5. Human salivary glands constitutively express CD14 and secrete as a soluble form in saliva.
|
