Oseko Fumishige, Yamamoto Toshiro, Akamatsu Yuki, Kanamura Narisato, Iwakura Yoichiro, Imanishi Jiro, Kita Masakazu
Department of Microbiology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Kamigyo-ku, Kyoto 602-8566, Japan.
Microbiol Immunol. 2009 May;53(5):287-94. doi: 10.1111/j.1348-0421.2009.00123.x. Epub 2009 Feb 9.
Periapical lesions are induced by bacterial infection of the dental pulp and result in destruction of the surrounding alveolar bone. Although various immunological studies concerning periapical bone resorption have been reported, the role of cytokines in the formation of periapical lesions remains unclear. In this study, the role of IL-17A in periapical lesions in mice was investigated. Normal C57BL/6, IFN-gamma(-/-), TNF-alpha(-/-), and IL-17A(-/-) mice were subjected to pulp exposure and infected with Prevotella intermedia (ATCC25611) and Porphyromonas gingivalis (ATCC33277) in the mandibular first molar. Periapical lesions were determined by muCT on day 21 after infection, and 3D visual construction was performed using 3D picture quantification software. The expression of IL-17A mRNA in periapical lesions was determined by the RT-PCR and real-time RT-PCR method. Periapical lesions developed in wild-type, IFN-gamma(-/-), and TNF-alpha(-/-) mice after infection with P. intermedia and P. gingivalis. However, periapical lesions were not observed in IL-17A(-/-) mice. The expression of IL-17A mRNA was significantly induced in periapical lesions of wild-type mice after infection. These results suggest that IL-17A, but not IFN-gamma or TNF-alpha, plays an important role in the formation of periapical lesions.
根尖周病变是由牙髓细菌感染引起的,会导致周围牙槽骨的破坏。尽管已经报道了各种关于根尖周骨吸收的免疫学研究,但细胞因子在根尖周病变形成中的作用仍不清楚。在本研究中,研究了IL-17A在小鼠根尖周病变中的作用。将正常的C57BL/6、IFN-γ(-/-)、TNF-α(-/-)和IL-17A(-/-)小鼠的下颌第一磨牙牙髓暴露,并感染中间普氏菌(ATCC25611)和牙龈卟啉单胞菌(ATCC33277)。感染后第21天通过微计算机断层扫描(muCT)确定根尖周病变,并使用3D图像定量软件进行三维可视化构建。通过逆转录聚合酶链反应(RT-PCR)和实时RT-PCR方法测定根尖周病变中IL-17A mRNA的表达。野生型、IFN-γ(-/-)和TNF-α(-/-)小鼠在感染中间普氏菌和牙龈卟啉单胞菌后出现根尖周病变。然而,在IL-17A(-/-)小鼠中未观察到根尖周病变。感染后野生型小鼠根尖周病变中IL-17A mRNA的表达明显诱导。这些结果表明,IL-17A而非IFN-γ或TNF-α在根尖周病变的形成中起重要作用。