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用SRL172(热灭活的母牛分枝杆菌)进行预接种可抑制Wistar大鼠的实验性牙周病。

Prevaccination with SRL172 (heat-killed Mycobacterium vaccae) inhibits experimental periodontal disease in Wistar rats.

作者信息

Breivik T, Rook G A

机构信息

Department of Periodontology, Faculty of Dentistry, University of Oslo, Oslo, Norway.

出版信息

Clin Exp Immunol. 2000 Jun;120(3):463-7. doi: 10.1046/j.1365-2249.2000.01231.x.

DOI:10.1046/j.1365-2249.2000.01231.x
PMID:10844524
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1905556/
Abstract

Periodontal disease is a bacterial dental plaque-induced destructive inflammatory condition of the tooth-supporting tissues, which is thought to be mediated by T lymphocytes secreting T helper 2 (Th2) cytokines, resulting in recruitment of high numbers of antibody-producing B lymphocytes/plasma cells as well as polymorphonuclear leucocytes (PMN) secreting tissue-destructive components, such at matrix metalloproteinases and reactive oxygen metabolites into the gingival connective tissues. One treatment strategy may be to down-regulate the Th2 response to those dental plaque microorganisms which induce the destructive inflammatory response. In this study we have examined the effects of a potent down-regulator of Th2 responses on ligature-induced periodontal disease in an experimental rat model. A single s.c. injection into Wistar rats of 0.1 or 1 mg of SRL172, a preparation of heat-killed Mycobacterium vaccae (NCTC 11659), 13 days before application of the ligature, significantly reduced the subsequent destruction of the tooth-supporting tissues, as measured by loss of periodontal attachment fibres (P < 0.001) and bone (P < 0.002). This protective effect occurred not only on the experimental (ligatured) side but also on the control unligatured side. SRL172 has undergone extensive toxicological studies and safety assessments in humans, and it is suggested that it may provide a safe and novel therapeutic approach to periodontal disease.

摘要

牙周病是一种由细菌牙菌斑引起的牙齿支持组织的破坏性炎症性疾病,被认为是由分泌辅助性T细胞2(Th2)细胞因子的T淋巴细胞介导的,导致大量产生抗体的B淋巴细胞/浆细胞以及分泌组织破坏性成分(如基质金属蛋白酶和活性氧代谢产物)的多形核白细胞(PMN)募集到牙龈结缔组织中。一种治疗策略可能是下调对那些诱导破坏性炎症反应的牙菌斑微生物的Th2反应。在本研究中,我们在实验性大鼠模型中研究了一种强效的Th2反应下调剂对结扎诱导的牙周病的影响。在结扎前13天,对Wistar大鼠皮下注射一次0.1或1mg的SRL172(一种热灭活的母牛分枝杆菌制剂(NCTC 11659)),通过牙周附着纤维丧失(P < 0.001)和骨丧失(P < 0.002)测量,显著减少了随后牙齿支持组织的破坏。这种保护作用不仅发生在实验(结扎)侧,也发生在对照未结扎侧。SRL172已在人体中进行了广泛的毒理学研究和安全性评估,并且表明它可能为牙周病提供一种安全且新颖的治疗方法。

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本文引用的文献

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Glucocorticoids inhibit bioactive IL-12p70 production by in vitro-generated human dendritic cells without affecting their T cell stimulatory potential.糖皮质激素可抑制体外培养的人树突状细胞产生具有生物活性的IL-12p70,而不影响其刺激T细胞的潜能。
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