The effects of the role of cytokine stimulated capsular polysaccharide Actinobacillus actinomycetemcomitans in human gingival fibroblast and monocyte.

细胞因子刺激荚膜多糖放线放线杆菌对人牙龈成纤维细胞和单核细胞作用的影响。

• 批准号: 14571805
• 负责人: ISHIHARA Yuichi
• 金额: $ 2.18万
• 依托单位: Aichi-Gakuin University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571805/
• 关键词: Actinobacillus actinomycetemcomitans_; polysaccharide; LPS; interleukin-6; interleukin-8; periodontitis; HGF; LPS; A.actinomycetemcomitans; 歯肉線維芽細胞; Interleukin-8; リポ多糖

We previously reported that a capsular polysaceharide (CP) from Actinobacillus actinomycetemcomitans Y4 induces bone resorption in a mouse organ culture system and osteoclast formation in mouse bone marrow cultures. However, the effects of A. actinomycetemcomitans Y4 CP on human gingival fibroblasts (HGF) are still unclear. The present study was undertaken to test the hypothesis that A. actinomycetemcomitans Y4 CP alters the production of inflammatory cytokines, such as interleukin-6 (IL-6) and IL-8 by HGF. When HGF were cultured with various concentrations of Y4 CP for 24 h, IL-6 and IL-8 production decreased in a concentration-dependent manner. Y4 CP (100 microg/ml) suppressed the release of IL-6 from 9.09 +/-0.08 ng/ml to 0.34 +/-0.21 ng/ml (P<0.01) and IL-8 production decreased from 3.76 +/-0.03 ng/ml to 0.09 +/-0.01 ng/ml (P<0.01). Y4 CP suppressed 70-80% of the release of IL-6 and IL-8 from HGF stimulated with Y4 lipopolysaccharide (LPS), too. Interestingly, anti-A. actinomycetemcomitans Y4 CP completely inhibited the effect of A. actinomycetemcomitans Y4 CP on IL-6 and IL-8 production from HGF. These results indicate that Y4 CP inhibits the release of IL-6 and IL-8 from HGF, suggesting that A. actinomycetemcomitans Y4 modulates the inflammatory response in periodontitis. Remarkably, this inhibitory effect was reversed by specific anti-A. actinomycetemcomitans Y4 CP suggesting an important relationship between the organism and the humoral host response.

我们以前报道过，从放线放线杆菌Y 4荚膜多糖（CP）诱导骨吸收在小鼠器官培养系统和破骨细胞形成在小鼠骨髓培养。然而，A.伴放线菌Y 4 CP对人牙龈成纤维细胞（HGF）的影响尚不清楚。本研究的目的是验证A.伴随放线菌Y 4 CP改变HGF产生炎性细胞因子，如白细胞介素-6（IL-6）和IL-8。当HGF与不同浓度的Y 4 CP共同培养24 h时，IL-6和IL-8的产生呈浓度依赖性下降。Y 4 CP（100 μ g/ml）抑制IL-6的释放，从9.09 ± 0.08 ng/ml降至0.34 ± 0.21 ng/ml（P<0.01），IL-8的产生从3.76 ± 0.03 ng/ml降至0.09 ± 0.01 ng/ml（P<0.01）。Y_4 CP也能抑制Y_4脂多糖（LPS）刺激的HGF释放IL-6和IL-8的70-80%。有趣的是，抗A。伴放线菌Y 4 CP完全抑制A.伴放线菌Y 4 CP对HGF产生IL-6和IL-8的影响。这些结果表明，Y 4 CP抑制HGF释放IL-6和IL-8，提示A.伴放线菌Y 4调节牙周炎的炎症反应。值得注意的是，这种抑制作用被特异性抗A逆转。放线菌共生菌Y 4 CP表明生物体和体液宿主反应之间的重要关系。

项目成果

Koide M. et al.: "Identification of the functional domain of osteoclast inhibitory nentide-1/hSca."J. Bone Miner Research. 17. 111-118 (2002)

Koide M. 等人：“破骨细胞抑制性 nentide-1/hSca 功能域的鉴定”。

Koide M, Maeda H, Reddy SV, et al.: "Identification of the functional domain of osteoclast inhibitory peptide-1/hSca."Journal Bone Mineral Research. 17(1). 111-118 (2002)

Koide M、Maeda H、Reddy SV 等人：“破骨细胞抑制肽-1/hSca 功能域的鉴定”。《骨矿物质研究杂志》。

Ohguchi Y, Ishihara Y, Noguchi T et al.: "Capsular polysaccharide from Actinobacillus actinomycetemcomitans inhibits IL-6 and IL-8 production in human gingival fibroblast."Journal of Pefiodontal Research. 38. 1-8 (2003)

Ohguchi Y、Ishihara Y、Noguchi T 等人：“来自 Actinobacillus actinomycetemcomitans 的荚膜多糖抑制人牙龈成纤维细胞中 IL-6 和 IL-8 的产生。”Pefiodontal Research 杂志。

Ishihara Y, Zhang JB, Tew JG et al.: "Non-redundant roles for interleukin-1 α and interleukin-1 β in regulating human IgG2"Journal of Periodontology. 72(10). 1332-1339 (2001)

Ishihara Y、Zhang JB、Tew JG 等人：“白细胞介素 1 α 和白细胞介素 1 β 在调节人 IgG2 中的非冗余作用”牙周病学杂志 72(10) 1332-1339。

Ishihara Y. et al.: "Monocyte differentiation in localized juvenile periodontitis is skewed toward the dendritic cell phenotype."Infection and Immunity. 70(6). 2780-2786 (2002)

Ishihara Y. 等人：“局部青少年牙周炎中的单核细胞分化偏向树突状细胞表型。”感染和免疫。