The distribution and expression of S100A8 and S100A9 in gingival epithelium of mice
The distribution and expression of S100A8 and S100A9 in gingival epithelium of mice
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DOI：
10.1111/jre.12000
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发表时间：
2013-04-01
影响因子：
3.5
通讯作者：
Yamamoto, M.
中科院分区：
文献类型：
--
作者：
Nishii, K.;Usui, M.;Yamamoto, M.
目的和背景牙龈上皮通过产生钙保护蛋白等抗菌肽来抵抗细菌感染。钙保护蛋白由蛋白S100A8和S100A9组成。虽然体外实验表明中性粒细胞和牙龈上皮细胞表达钙保护蛋白，但体内对S100A8和S100A9蛋白在牙龈组织中的表达和两种S100蛋白的共定位尚不完全清楚。本研究旨在探讨有无感染情况下S100A8和S100A9在小鼠牙龈上皮中的表达分布。材料与方法采用激光显微解剖和实时聚合酶链反应（PCR）技术，定量分析无菌小鼠和常规小鼠口腔粘膜上皮（JE）和口腔龈上皮（OGE）中S100A8和S100A9 mRNA的表达。采用荧光免疫组织化学方法证实S100A8和S100A9 mRNA在乙脑中的表达。结果实时荧光定量PCR结果显示，S100A8和S100A9主要在乙脑中检测到，而在OGE中仅少量或未检测到。常规小鼠乙脑中S100A8和S100A9 mRNA表达水平均显著高于无菌小鼠乙脑。此外，荧光免疫组化显示，S100A8在常规小鼠和无菌小鼠的乙脑中均有表达，而S100A9在常规小鼠的乙脑中均有表达，而无菌小鼠的乙脑中无表达。结论S100A8蛋白在口腔细菌感染和未感染的小鼠乙脑细胞中均有表达。存在微生物菌群时，S100A9在乙脑细胞中的表达明显高于无微生物菌群时，提示S100A9的表达可能受微生物菌群感染的诱导。牙龈上皮细胞钙保护蛋白的产生可能是通过细菌感染诱导的S100A9介导的。
Objective and Background Gingival epithelium protects against bacterial infection by producing antimicrobial peptides such as calprotectin. Calprotectin consists of proteins S100A8 and S100A9. Although in vitro assay has shown that neutrophils and gingival epithelial cells express calprotectin, the expression of S100A8 and S100A9 and colocalization of both S100 proteins in gingival tissue in vivo are not fully understood. The aim of this study was to investigate the distribution of S100A8 and S100A9 expression in gingival epithelium of mice in the presence and absence of infection. Materials and Methods A quantitative analysis of S100A8 and S100A9 mRNA in junctional epithelium (JE) and oral gingival epithelium (OGE) of both germ-free mice and conventional mice was performed using laser microdissection and real-time polymerase chain reaction (PCR). Confirmation of S100A8 and S100A9 mRNA expression in the JE was conducted by fluorescent immunohistochemistry. Results Real-time PCR analysis indicated that S100A8 and S100A9 expressions were mainly detected in JE and only slightly or not detected in OGE. Levels of both S100A8 and S100A9 mRNA expression in JE of conventional mice were significantly higher than those in JE of germ-free mice. Additionally, fluorescent immunohistochemistry showed that S100A8 expression was observed in the JE of both conventional and germ-free mice, whereas S100A9 was expressed in the JE of conventional but not germ-free mice. Conclusion S100A8 protein is expressed in JE cells of mice in the presence and in the absence of infection with oral bacteria. S100A9 expression in JE cells in the presence of microflora is significantly increased compared with the absence of microflora, which suggests that S100A9 expression may be induced by infection of microflora. The production of calprotectin in gingival epithelial cells may be mediated through S100A9 induction by bacterial infection.