Protective role of osteopontin in endodontic infection.

Protective role of osteopontin in endodontic infection.
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骨桥蛋白在牙髓感染中的保护作用。

DOI:
10.1111/j.1365-2567.2009.03159.x
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发表时间:
2010
期刊:
影响因子:
6.4
通讯作者:
Sasaki,Hajime
Sasaki,Hajime
中科院分区:
医学2区
文献类型:
--
作者:
Rittling,SusanR;Zetterberg,Craig;Yagiz,Kader;Skinner,Stephen;Suzuki,Noriyuki;Fujimura,Akira;Sasaki,Hajime

文献摘要

相似文献

牙髓感染是多种微生物感染,导致骨破坏和牙齿脱落。宿主对这些感染的反应是复杂的,包括先天和适应性机制。骨桥蛋白(OPN)是一种分泌的整合素结合蛋白,在调节免疫应答和增强白细胞迁移中发挥作用。我们已经使用一个良好表征的小鼠模型评估了OPN在宿主对牙髓感染的反应中的作用。与感染后3周的野生型相比,OPN缺陷小鼠中与牙髓感染相关的根尖周骨丢失显著更严重,并且与炎症面积增加相关。感染后3天,与骨丢失相关的细胞因子白细胞介素-1 α(IL-1α)和RANKL的表达增加。OPN缺乏对这些感染的适应性免疫应答几乎没有影响,因为基因型对感染小鼠血清中细菌特异性免疫球蛋白G1和G2 a的比例没有影响。此外,与辅助性T细胞1型/2型平衡相关的细胞因子:IL-12,IL-10和干扰素-γ的表达没有差异。在感染组织中,感染后3天,OPN缺陷动物病变区域的中性粒细胞浸润轻微增加:这通过该时间点OPN缺陷样本中中性粒细胞弹性蛋白酶表达的显著增加得到证实。 我们得出结论,骨桥蛋白对多种微生物感染具有保护作用,至少部分是因为吞噬细胞募集和/或感染部位持久性的改变,并且这种分子在多种微生物感染中具有潜在的治疗作用。
Endodontic infections are polymicrobial infections resulting in bone destruction and tooth loss. The host response to these infections is complex, including both innate and adaptive mechanisms. Osteopontin (OPN), a secreted, integrin‐binding protein, functions in the regulation of immune responses and enhancement of leucocyte migration. We have assessed the role of OPN in the host response to endodontic infection using a well‐characterized mouse model. Periapical bone loss associated with endodontic infection was significantly more severe in OPN‐deficient mice compared with wild‐type 3 weeks after infection, and was associated with increased areas of inflammation. Expression of cytokines associated with bone loss, interleukin‐1α (IL‐1α) and RANKL, was increased 3 days after infection. There was little effect of OPN deficiency on the adaptive immune response to these infections, as there was no effect of genotype on the ratio of bacteria‐specific immunoglobulin G1 and G2a in the serum of infected mice. Furthermore, there was no difference in the expression of cytokines associated with T helper type 1/type2 balance: IL‐12, IL‐10 and interferon‐γ. In infected tissues, neutrophil infiltration into the lesion area was slightly increased in OPN‐deficient animals 3 days after infection: this was confirmed by a significant increase in expression of neutrophil elastase in OPN‐deficient samples at this time‐point. We conclude that OPN has a protective effect on polymicrobial infection, at least partially because of alterations in phagocyte recruitment and/or persistence at the sites of infection, and that this molecule has a potential therapeutic role in polymicrobial infections.