Response of epithelial cells infected by Treponema denticola

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K11461
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: Tokyo Dental College
• Principal Investigator: Eitoyo Kokubu 東京歯科大学, 歯学部, 講師 (70453785)
• Co-Investigator(Kenkyū-buntansha): 石原 和幸 東京歯科大学, 歯学部, 教授 (00212910) ; 菊池 有一郎 東京歯科大学, 歯学部, 講師 (30410418)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: Treponema denticola / 細胞侵入 / サイトカイン / 歯周病 / 免疫応答

Outline of Final Research Achievements

To clarify the pathogenicity of T. denticola, epithelial cells were infected with the wild-type strain or a mutant strain deficient in dentilisin or a major outer sheath protein (ΔprtP or Δmsp respectively). The migration activity of cells infected by ΔprtP compared with those infected by wild-type strain and Δmsp. TLR-2 signal intensity was greater in the cells infected by ΔprtP than in cells infected by the wild-type strain.
These results indicate that prtP modulates pathogen recognition via TLR2 and that dentilisin has the potential to degrade paxillin and HSP70, which decreases cell migration and delays stress response. Collectively, the findings show that prtP modulates the immune response of host cells to T. denticola infection.

Free Research Field

微生物学

Academic Significance and Societal Importance of the Research Achievements

本研究によりT. denticolaの病原性因子による口腔粘膜上皮組織への感染および細胞侵入のメカニズムが明らかになる。本菌の病原性の解明および宿主免疫に対する回避機構は、慢性歯周病疾患の機序の解明や口腔内細菌の侵入予防への応用の糸口となる。さらに本菌の構成成分であるMspは、梅毒の病原体であるTreponema pallidamとの遺伝学的に相同分子があることが知られているため、本研究の成果は、歯周病の病原性に限局されず、Treponema属全体の病原性メカニズムの解析につながり、梅毒あるいはDigital dermatitis等のTreponema感染症の治療に繋がる。