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[牙周病细菌提取物对人牙龈角质形成细胞的多形核白细胞介导作用]

[Polymorphonuclear leukocyte-mediated effects on human oral keratinocytes by periodontopathic bacterial extracts].

作者信息

Sugiyama E

机构信息

Department of Periodontology, Faculty of Dentistry, Tokyo Medical and Dental University.

出版信息

Kokubyo Gakkai Zasshi. 1992 Mar;59(1):75-87. doi: 10.5357/koubyou.59.75.

Abstract

In order to investigate the polymorphonuclear leukocyte-mediated oral keratinocyte injury, the author established a method to culture keratinocytes (SCC9 and gingival keratinocytes) and subjected to the cell detachment assay by polymorphonuclear leukocytes and/or bacterial ultrasonic extracts from Actinobacillus actinomycetemcomitans Y4, Bacteroides forsythus OMZ 408, Fusobacterium nucleatum ATCC 10953, Capnocytophaga sputigena 4 and Eikenella corrodens 1073. The bacterial extracts alone caused no cell disruption of the keratinocyte monolayers. Polymorphonuclear leukocyte alone caused only a minimal cell detachment. On the contrary, when the bacterial extracts were added to the co-culture of keratinocytes and polymorphonuclear leukocytes, cell detachment of keratinocytes was observed except for the bacterial extract from Eikenella corrodens 1073. The effect of Actinobacillus actinomycetemcomitans Y4 was the strongest. This effect was heat labile and not inhibited by polymyxin B. Cell detachment was inhibited by alpha 1-antitrypsin but not by catalase and superoxide dismutase. No keratinocyte lysis was observed in terms of 51Cr release. Hydrogen peroxide and leukocyte elastase also caused keratinocyte detachment. These results indicate that polymorphonuclear leukocyte can cause non-lytic cell detachment of the gingival keratinocytes when encountering some bacteria, which may lead to the increase of the permeability of the keratinocyte layers.

摘要

为了研究多形核白细胞介导的口腔角质形成细胞损伤,作者建立了角质形成细胞(SCC9和牙龈角质形成细胞)的培养方法,并通过多形核白细胞和/或来自伴放线放线杆菌Y4、福赛坦氏拟杆菌OMZ 408、具核梭杆菌ATCC 10953、产黑色素普雷沃菌4和腐蚀艾肯菌1073的细菌超声提取物进行细胞脱离试验。单独的细菌提取物未引起角质形成细胞单层的细胞破坏。单独的多形核白细胞仅引起最小程度的细胞脱离。相反,当将细菌提取物添加到角质形成细胞和多形核白细胞的共培养物中时,除了来自腐蚀艾肯菌1073的细菌提取物外,观察到角质形成细胞的细胞脱离。伴放线放线杆菌Y4的作用最强。这种作用对热不稳定,且不受多粘菌素B抑制。细胞脱离受α1-抗胰蛋白酶抑制,但不受过氧化氢酶和超氧化物歧化酶抑制。就51Cr释放而言,未观察到角质形成细胞裂解。过氧化氢和白细胞弹性蛋白酶也导致角质形成细胞脱离。这些结果表明,多形核白细胞在遇到某些细菌时可导致牙龈角质形成细胞发生非溶解性细胞脱离,这可能导致角质形成细胞层通透性增加。

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