2007 Fiscal Year Final Research Report Summary
The elucidation of salivary histatin, in correlation with survival and reproduction of oral cells, and Toll-like receptor signals
| Project/Area Number |
18592051
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Matsumoto Dental University |
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Principal Investigator |
IMAMURA Yasuhiro Matsumoto Dental University, School of Dentistry, Assistant Prof. (00339136)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIGAKI Yoshihisa Matsumoto Dental Univ., School of Dentistry, Research Associate (80367523)
WANG Pao-Li Matsumoto Dental Univ., School of Dentistry, Prof. (20213613)
UDAGAWA Nobuyuki Matsumoto Dental Univ., School of Dentistry, Prof. (70245801)
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| Project Period (FY) |
2006 – 2007
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| Keywords | salivary protein / histatin / Toll-like receptor |
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| Research Abstract |
An environmental factor is mentioned as an etiology of periodontal diseases. It causes destruction of adhesion between teeth and soft tissue. And the connective and haul tissue hire as the alveolar bone can be also destruction. This behavior is induced chronic inflammation by the complicated interaction between host cells. Histatins are salivary proteins relative to innate immune system, which have an anti-C anima activity, growth inhibition of S.mutans and inactivation of collagenase from periodontal pathogens. The function of histatins against host, in particular oral cells, has not been understood sofar. We have studied that histatin is entned by endocytosis in human gingivalfibmblasts (HGF) and Lards to heat shockprotein HSC70. The histatin/HSC70 compiex is slightly and thematically traaslocated into nudeus at physiological and heat shocked conditions, respectively. And histatin is also enhanted both DNA synthesis and cellviability.in HGF.
Toll-like receptors (TLRs) are relative to innate immune system. Several HSPs works as ligands against TLRs. However it has not been clarified whether HSC70 also becomes a ligand. When 293-TLRA/CD14-MD-2 cells, constitutive expression of TLR4, CD14 and MD-2, were stimulated with HSC70, NF-κB was activated Moreoveg histathr/HSC70 complex was not served as the ligand anylonget The resuk suggests that histatin prevents the role of ligand of HSC70 about TLR4. It implies the possibility that histatin. Is an anti-inflammatory factor preventing the production of inflammatory cytokines through the NW-κB adivation. The present findings provide new clues far our understanding of the mechanisms afinnate imaramoresponce in oral cavity folowedby development for antifimgal and anti-inflammatory drug or reproduction aforal tissues (cells) by salivary protein histatin.
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