Periodontal Biology Laboratory, Faculty of Dentistry, Universidad de Chile, Santiago, Chile.
Molecular Immunology Laboratory, Faculty of Biological Sciences, Universidad de Concepción, Concepción, Chile.
J Periodontol. 2018 Oct;89(10):1249-1261. doi: 10.1002/JPER.17-0563. Epub 2018 Aug 20.
Aggregatibacter actinomycetemcomitans expresses several virulence factors that may contribute to the pathogenesis of periodontitis. Based on the antigenicity of the O-polysaccharide component of the lipopolysaccharide (LPS), different A. actinomycetemcomitans serotypes have been described. Among them, serotype b has demonstrated a stronger capacity to trigger Th1 and Th17-associated cytokine, CC-chemokine, and CC-chemokine receptor production on immune cells in vitro. With a murine model of experimental periodontitis, this investigation aimed to analyze the alveolar bone resorption and the pattern of immune response triggered by the different A. actinomycetemcomitans serotypes within periodontal lesions.
For periodontal lesion induction, mice were orally infected with the different A. actinomycetemcomitans serotypes or their purified LPS. Alveolar bone resorption was analyzed using microcomputed tomography and scanning electron microscopy. Bacterial infection, receptor activator of nuclear factor-kappa B ligand (RANKL) and Th1 and Th17-associated cytokine, CC-chemokine, and CC-chemokine receptor levels were quantified by quantitative polymerase chain reaction (qPCR). T lymphocytes isolated from periodontal lesions were analyzed by flow cytometry.
In periodontal lesions, serotype b of A. actinomycetemcomitans induced higher alveolar bone resorption and expression of RANKL compared with the other serotypes. In addition, serotype b induced greater levels of Th1- and Th17-related cytokines, CC-chemokines, and CC-chemokine receptors than the others. Similarly, higher numbers of infiltrating Th1 and Th17 lymphocytes were detected in serotype b-induced periodontal lesions.
These results demonstrate that periodontal lesions induced with different A. actinomycetemcomitans serotypes elicited distinct alveolar bone resorption and immune response. In particular, serotype b was more pathogenic than the others and induced stronger Th1 and Th17 patterns of immune responses during experimental periodontitis.
伴放线放线杆菌表达多种毒力因子，这些因子可能与牙周炎的发病机制有关。根据脂多糖（LPS）的 O-多糖成分的抗原性，已经描述了不同的伴放线放线杆菌血清型。其中，血清型 b 已被证明在体外对免疫细胞具有更强的触发 Th1 和 Th17 相关细胞因子、CC-趋化因子和 CC-趋化因子受体产生的能力。本研究通过实验性牙周炎的小鼠模型，旨在分析不同血清型伴放线放线杆菌在牙周病变中引发的牙槽骨吸收和免疫反应模式。
为了诱导牙周病损，小鼠经口感染不同的伴放线放线杆菌血清型或其纯化 LPS。使用微计算机断层扫描和扫描电子显微镜分析牙槽骨吸收。通过定量聚合酶链反应（qPCR）定量检测细菌感染、核因子 κB 配体（RANKL）和 Th1 和 Th17 相关细胞因子、CC-趋化因子和 CC-趋化因子受体水平。通过流式细胞术分析从牙周病损中分离的 T 淋巴细胞。
在牙周病损中，与其他血清型相比，伴放线放线杆菌血清型 b 诱导更高的牙槽骨吸收和 RANKL 表达。此外，与其他血清型相比，血清型 b 诱导更高水平的 Th1 和 Th17 相关细胞因子、CC-趋化因子和 CC-趋化因子受体。同样，在血清型 b 诱导的牙周病损中检测到更多浸润的 Th1 和 Th17 淋巴细胞。
这些结果表明，用不同的伴放线放线杆菌血清型诱导的牙周病损引起了不同的牙槽骨吸收和免疫反应。特别是，血清型 b 比其他血清型更具致病性，并在实验性牙周炎中诱导更强的 Th1 和 Th17 免疫反应模式。
