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牙龈卟啉单胞菌和齿密螺旋体协同增强牙周炎小鼠模型的毒力。

Synergistic virulence of Porphyromonas gingivalis and Treponema denticola in a murine periodontitis model.

机构信息

Oral Health CRC, Melbourne Dental School and Bio21 Institute, The University of Melbourne, Melbourne, Vic., Australia.

出版信息

Mol Oral Microbiol. 2011 Aug;26(4):229-40. doi: 10.1111/j.2041-1014.2011.00612.x. Epub 2011 May 2.

DOI:10.1111/j.2041-1014.2011.00612.x
PMID:21729244
Abstract

Chronic periodontitis is characterized by the destruction of the tissues supporting the teeth and has been associated with the presence of a subgingival polymicrobial biofilm containing Porphyromonas gingivalis and Treponema denticola. We have investigated the potential synergistic virulence of P. gingivalis and T. denticola using a murine experimental model of periodontitis. An inoculation regime of four intra-oral doses of 1 × 10(10) P. gingivalis cells induced significant periodontal bone loss compared with loss in sham-inoculated mice, whereas doses of 1 × 10(9) cells or lower did not induce bone loss. Inoculation with T. denticola with up to eight doses of 1 × 10(10) cells failed to induce bone loss in this model. However, four doses of a co-inoculum of a 1 : 1 ratio of P. gingivalis and T. denticola at 5 × 10(8) or 1 × 10(9) total bacterial cells induced the same level of bone loss as four doses of 1 × 10(10) P. gingivalis cells. Co-inoculation induced strong P. gingivalis-specific T-cell proliferative and interferon-γ-dominant cytokine responses, and induced a strong T. denticola-specific interferon-γ dominant cytokine response. Only at the higher co-inoculum dose of 1 × 10(10) total cells was a T. denticola-specific T-cell proliferative response observed. These data show that P. gingivalis and T. denticola act synergistically to stimulate the host immune response and to induce alveolar bone loss in a murine experimental periodontitis model.

摘要

慢性牙周炎的特征是牙齿支持组织的破坏,并与含有牙龈卟啉单胞菌和密螺旋体的龈下多微生物生物膜的存在有关。我们使用牙周炎的实验性啮齿动物模型研究了牙龈卟啉单胞菌和密螺旋体的潜在协同毒力。与假接种小鼠相比,四次口腔内 1 × 10(10) 个牙龈卟啉单胞菌细胞的接种方案诱导了明显的牙周骨丢失,而 1 × 10(9) 个或更低剂量的细胞则不会诱导骨丢失。在该模型中,用多达 8 次 1 × 10(10) 个细胞的密螺旋体接种也不能诱导骨丢失。然而,5 × 10(8) 或 1 × 10(9) 总细菌细胞的 1:1 比例的牙龈卟啉单胞菌和密螺旋体共接种物的四次剂量诱导了与四次 1 × 10(10) 个牙龈卟啉单胞菌细胞相同水平的骨丢失。共接种诱导了强烈的牙龈卟啉单胞菌特异性 T 细胞增殖和干扰素-γ占主导地位的细胞因子反应,并诱导了强烈的密螺旋体特异性干扰素-γ占主导地位的细胞因子反应。只有在较高的共接种物剂量 1 × 10(10) 总细胞时,才观察到密螺旋体特异性 T 细胞增殖反应。这些数据表明,牙龈卟啉单胞菌和密螺旋体协同作用,刺激宿主免疫反应,并在实验性牙周炎啮齿动物模型中诱导牙槽骨丢失。

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