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首页> 外文期刊>Clinical and diagnostic laboratory immunology >Gamma Interferon (IFN-γ) and IFN-γ-Inducing Cytokines Interleukin-12 (IL-12) and IL-18 Do Not Augment Infection-Stimulated Bone Resorption In Vivo
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Gamma Interferon (IFN-γ) and IFN-γ-Inducing Cytokines Interleukin-12 (IL-12) and IL-18 Do Not Augment Infection-Stimulated Bone Resorption In Vivo

机译：γ干扰素（IFN-γ）和IFN-γ诱导细胞因子白介素12（IL-12）和IL-18不会增强感染刺激的体内骨吸收。

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Periapical granulomas are induced by bacterial infection of the dental pulp and result in destruction of the surrounding alveolar bone. In previous studies we have reported that the bone resorption in this model is primarily mediated by macrophage-expressed interleukin-1 (IL-1). The expression and activity of IL-1 is in turn modulated by a network of Th1 and Th2 regulatory cytokines. In the present study, the functional roles of the Th1 cytokine gamma interferon (IFN-γ) and IFN-γ-inducing cytokines IL-12 and IL-18 were determined in a murine model of periapical bone destruction. IL-12?/?, IL-18?/?, and IFN-γ?/? mice were subjected to surgical pulp exposure and infection with a mixture of four endodontic pathogens, and bone destruction was determined by microcomputed tomography on day 21. The results indicated that all IL-12?/?, IL-18?/?, and IFN-γ?/? mice had similar infection-stimulated bone resorption in vivo as wild-type control mice. Mice infused with recombinant IL-12 also had resorption similar to controls. IFN-γ?/? mice exhibited significant elevations in IL-6, IL-10, IL-12, and tumor necrosis factor alpha in lesions compared to wild-type mice, but these modulations had no net effect on IL-1α levels. Recombinant IL-12, IL-18, and IFN-γ individually failed to consistently modulate macrophage IL-1α production in vitro. We conclude that, at least individually, endogenous IL-12, IL-18, and IFN-γ do not have a significant effect on the pathogenesis of infection-stimulated bone resorption in vivo, suggesting possible functional redundancy in proinflammatory pathways.
机译：根尖肉芽肿是由牙髓的细菌感染引起的，并导致周围牙槽骨的破坏。在以前的研究中，我们已经报道了该模型中的骨吸收主要是由巨噬细胞表达的白介素1（IL-1）介导的。 IL-1的表达和活性又受Th1和Th2调节性细胞因子网络的调节。在本研究中，在小鼠根尖周骨破坏模型中确定了Th1细胞因子γ干扰素（IFN-γ）和IFN-γ诱导细胞因子IL-12和IL-18的功能作用。对IL-12 ？/？，IL-18 ？/？和IFN-γ？/？小鼠进行手术牙髓暴露，在第21天，用四种牙髓病原体的混合物感染，并通过显微计算机断层扫描确定骨破坏。结果表明，所有IL-12 α/β，IL-18 α/β< / sup>和IFN-γ？/？小鼠体内的感染刺激骨吸收与野生型对照小鼠相似。注入重组IL-12的小鼠也具有与对照相似的吸收。与野生型小鼠相比，IFN-γ？/？小鼠的病灶中IL-6，IL-10，IL-12和肿瘤坏死因子α明显升高，但这些调节没有净对IL-1α水平的影响。重组IL-12，IL-18和IFN-γ分别不能始终如一地调节体外巨噬细胞IL-1α的产生。我们得出的结论是，至少在个体上，内源性IL-12，IL-18和IFN-γ对感染刺激的体内骨吸收的发病机理没有显着影响，提示促炎途径中可能存在功能冗余。

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