Immunological and molecular biological study of cytokine-network in periodontitis

牙周炎细胞因子网络的免疫学和分子生物学研究

• 批准号: 09470418
• 负责人: ISHIKAWA Isao
• 金额: $ 9.41万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (B).
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-09470418/
• 关键词: IL-12; IFN-g; periodontitis; Th1; monocyte; IFN-g; COX-2; IL-1; IL-4; CD14; 歯周疾患; P.gingivalis

We have examined local and systematic function of cytokines against periodontopathic bacteria to clarify cytokine-network in periodontitis.Helper T cells, which regulate immune responses, have been divided into Type1 helper T cell(Th1)and Type2 helper T cell(Th2). Th1 augments cell-mediated immune responses, and Th2 helps humoral immune responses. This difference is determined by cytokine production, for example, Th1 produces IFN-γ and IL-2, Th2 produces IL-4, IL-5, IL-6 and IL-10. The aim of our study in this year was to examine whether individual diversities exist on not in immune responses against periodontopathic bacteria, and how individual diversities affect the clinical status in periodontitis.Periheral blood T cells produce IFN-γ by stimulation with periodontopathic bacteria. IFN-γ production varied among individuals. The production of IFN-γ was dependent on the ability of monocytes to produce IL-12.As the severity of periodontitis was not different between IFN-γ high and low producer, we could not determine the susceptibility of periodontitis based on the polarization of Th1 or Th2, although immune response against periodontopathic bacteria varied among individuals.

为了阐明细胞因子在牙周炎中的细胞因子网络，我们研究了细胞因子在牙周病中的局部和系统作用。辅助T细胞调节免疫反应，分为1型辅助T细胞(Th1)和2型辅助T细胞(Th2)。Th1增强细胞免疫应答，Th2帮助体液免疫应答。这种差异是由细胞因子的产生决定的，例如Th1产生干扰素-γ和IL-2，Th2产生IL-4、IL-5、IL-6和IL-10。我们今年的研究目的是探讨牙周病细菌的免疫反应是否存在个体差异，以及个体差异如何影响牙周炎的临床状态。干扰素-γ的产生因个体而异。干扰素-γ的产生依赖于单核细胞产生IL-12的能力，由于干扰素-γ的高、低分泌水平对牙周炎的严重程度没有差别，因此我们不能根据Th1或Th2的极化来确定牙周炎的易感性，尽管对牙周病细菌的免疫反应因人而异。

项目成果

Noguchi K, Iwasaki K, Endo H, Kondo H, Shitashige M, Ishikawa I.: "Prostaglandin E2 and I2 downregulate tumor necrosis factor-a induced intercellular adhesion molecule-1 expression in human oral gingival epithelial cells."Oral Microbiol Immunol. 15. 299-3

Noguchi K、Iwasaki K、Endo H、Kondo H、Shitashige M、Ishikawa I.：“前列腺素 E2 和 I2 下调人口腔牙龈上皮细胞中肿瘤坏死因子 -a 诱导的细胞间粘附分子 -1 的表达。”口腔微生物免疫学。

Ono J.Nagasawa T.Aramaki M.Kobayashi H.Ishikawa I: "Periodontal status of a juvenile with selective IgA deliciency : a case report"Journal of the International Academy of Periodontology. 1. 16-20 (1999)

Ono J.Nagasawa T.Aramaki M.Kobayashi H.Ishikawa I：“具有选择性 IgA 美味的青少年的牙周状况：病例报告”国际牙周病学会杂志。

Nagasawa T: "Oral administration of Porphyromonas gingivalis fimbriae with cholera toxin induces anti-fimbriae serum IgG, IgM, IgA and salivary IgA antibodies."J Periodont Res. 33. 169-174 (1999)

Nagasawa T：“口服牙龈卟啉单胞菌菌毛和霍乱毒素可诱导抗菌毛血清 IgG、IgM、IgA 和唾液 IgA 抗体。”J periodont Res。

長澤敏行、石川烈: "歯周病学最前線"奥田克爾、我孫子宜光、石川烈、岡田宏、古賀敏比呂、野口俊英、村山洋二. 354 (2000)

Toshiyuki Nagasawa、Retsu Ishikawa：“牙周病学的前沿” Katsuji Okuda、Yoshimitsu Abiko、Retsu Ishikawa、Hiroshi Okada、Toshihiro Koga、Toshihide Noguchi、Yoji Murayama 354 (2000)。

林丈一郎、石川烈: "歯周病 新しい治療を求めて"岡田宏、石川烈、村山洋二. 530 (2000)

Joichiro Hayashi、Retsu Ishikawa：“牙周疾病：寻找新的治疗方法” Hiroshi Okada、Retsu Ishikawa、Yoji Murayama 530 (2000)。