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用变形链球菌59千道尔顿葡聚糖结合蛋白对大鼠进行实验性免疫可预防龋齿。

Experimental immunization of rats with a Streptococcus mutans 59-kilodalton glucan-binding protein protects against dental caries.

作者信息

Smith D J, Taubman M A

机构信息

Department of Immunology, Forsyth Dental Center, Boston, Massachusetts 02115, USA.

出版信息

Infect Immun. 1996 Aug;64(8):3069-73. doi: 10.1128/iai.64.8.3069-3073.1996.

Abstract

Glucan-binding proteins (GBPs) are theoretically important in the molecular pathogenesis of dental caries caused by Streptococcus mutans. The present study evaluated the ability of antibody induced by the S. mutans 59-kDa GBP (GBP59) to affect dental caries caused by experimental infection with S. mutans in a rodent model. Groups of 20-day-old rats were injected twice at 9-day intervals subcutaneously in the salivary gland vicinity with GBP59, glucosyltransferase (GTF), or phosphate-buffered saline (sham injection), each incorporated in an adjuvant. Two weeks after the second injection, GBP59- and GTF-injected rats contained significant levels of salivary immunoglobulin A and serum immunoglobulin G antibody to the respective injected antigens. However, cross-reacting antibody to S. mutans GTF or GBP59 was not induced by the respective antigen. Rats were then orally infected with S. mutans. After 71 days of infection, GBP59- and GTF-injected groups had smaller numbers of S. mutans on their molar surfaces, compared with the sham-injected infected group. Total, sulcal, and smooth-surface molar caries in the GBP59- and GTF-immunized S. mutans-infected groups were each significantly lower (P < or = 0.003) than the respective measures of caries in the sham injected infected group. The results of this investigation demonstrate that immunization with S. mutans GBP59 induces an immune response in rats that can interfere with the accumulation of S. mutans and can reduce the level of dental caries caused by this cariogenic streptococcus. Furthermore, the protective immunity induced by either GBP59 or GTF appears to result from antibodies to independent epitopes since these two S. mutans components do not have a close antigenic relationship.

摘要

葡聚糖结合蛋白(GBPs)在变形链球菌致龋的分子发病机制中具有重要的理论意义。本研究评估了由变形链球菌59-kDa葡聚糖结合蛋白(GBP59)诱导产生的抗体在啮齿动物模型中影响变形链球菌实验性感染所致龋齿的能力。将20日龄大鼠分组,每隔9天在唾液腺附近皮下注射一次GBP59、葡糖基转移酶(GTF)或磷酸盐缓冲盐水(假注射),每种均与佐剂混合。第二次注射两周后,注射GBP59和GTF的大鼠唾液免疫球蛋白A和血清免疫球蛋白G抗体针对各自注射抗原的水平显著升高。然而,相应抗原并未诱导出针对变形链球菌GTF或GBP59的交叉反应抗体。然后给大鼠经口感染变形链球菌。感染71天后,与假注射感染组相比,注射GBP59和GTF的组磨牙表面的变形链球菌数量较少。GBP59免疫组和GTF免疫组的变形链球菌感染大鼠的总磨牙龋、龈沟龋和平滑面龋均显著低于(P≤0.003)假注射感染组的相应龋病指标。本研究结果表明,用变形链球菌GBP59免疫可在大鼠中诱导免疫反应,该反应可干扰变形链球菌的聚集,并可降低这种致龋链球菌引起的龋齿水平。此外,GBP59或GTF诱导的保护性免疫似乎是由针对独立表位的抗体引起的,因为这两种变形链球菌成分没有密切的抗原关系。

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本文引用的文献

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Role of Streptococcus mutans in human dental decay.变形链球菌在人类龋齿中的作用。
Microbiol Rev. 1986 Dec;50(4):353-80. doi: 10.1128/mr.50.4.353-380.1986.

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