Immunohistochemical localization of IL-17 in induced rat periapical lesions.
Immunohistochemical localization of IL-17 in induced rat periapical lesions.
复制标题
DOI：
10.1016/j.joen.2008.10.022
复制
发表时间：
2009-02
影响因子：
4.2
通讯作者：
H. Xiong;Lili Wei;B. Peng
中科院分区：
文献类型：
--
作者：
H. Xiong;Lili Wei;B. Peng
白细胞介素（IL）-17是一种新的促炎细胞因子家族的成员，其几乎完全由新认识的称为“Th 17”细胞的活化T细胞亚类产生。从牙髓角度来看，IL-17有效地调节先天免疫系统的细胞，作为适应性和先天免疫系统之间的重要桥梁分子。本研究旨在探讨IL-17在大鼠根尖周病变发生发展过程中的免疫组织化学定位。SD大鼠下颌第一磨牙牙髓暴露后28天内发生根尖周病变。在牙髓暴露后0、7、14、21和28天随机处死动物。获取包含第一磨牙的颌骨，并常规制备用于组织学分析、免疫组织化学和酶组织化学。从第0天到第28天，IL-17阳性细胞和中性粒细胞的数量上升，并在第28天达到峰值。破骨细胞数量从第0天到第14天大量增加，然后从第14天到第28天逐渐减少。此外，破骨细胞减少与IL-17阳性细胞和中性粒细胞数量增加形成对比。提示IL-17可能参与根尖周组织的炎症反应和骨吸收，并与根尖周病变的发生发展有关。
Interleukin (IL)-17 is a member of a novel family of proinflammatory cytokines produced almost exclusively by a newly recognized subclass of activated T cells called “Th17” cells. From an endodontic perspective, IL-17 potently regulates cells of the innate immune system, serving as an important bridging molecule between the adaptive and innate immune systems. The purpose of this study was to investigate the immunohistochemical localization of IL-17 during the development of periapical lesions in rats. Periapical lesions developed within 28 days after mandibular first molar pulp exposure in Sprague-Dawley rats. The animals were randomly sacrificed at 0, 7, 14, 21, and 28 days after pulpal exposure. The jaws that contained the first molar were obtained and routinely prepared for histologic analysis, immunohistochemistry, and enzyme histochemistry. From day 0 to day 28, the number of IL-17–positive cells and neutrophils ascended and peaked on day 28. Osteoclast numbers substantially multiplied from day 0 to day 14 and then gradually decreased from day 14 to day 28. In addition, the osteoclast decrease contrasted with the increased number of IL-17–positive cells and neutrophils. These findings showed that IL-17 could be observed and might possibly be involved in the inflammatory response and bone resorption of periapical tissues as well as associated with periapical lesion pathogenesis.