The distribution and expression of S 100 A 8 and S 100 A 9 in gingival epithelium of mice

Objective and Background Gingival epithelium protects against bacterial infection by producing antimicrobial peptides such as calprotectin. Calprotectin consists of proteins S 100 A 8 and S 100 A 9. Although in vitro assay has shown that neutrophils and gingival epithelial cells express calprotectin, the expression of S 100 A 8 and S 100 A 9 and colocalization of both S 100 proteins in gingival tissue in vivo are not fully understood. The aim of this study was to investigate the distribution of S 100 A 8 and S 100 A 9 expression in gingival epithelium of mice in the presence and absence of infection. Materials and Methods A quantitative analysis of S 100 A 8 and S 100 A 9 m RNA 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 S 100 A 8 and S 100 A 9 m RNA expression in the JE was conducted by fluorescent immunohistochemistry. Results Real‐time PCR analysis indicated that S 100 A 8 and S 100 A 9 expressions were mainly detected in JE and only slightly or not detected in OGE . Levels of both S 100 A 8 and S 100 A 9 m RNA expression in JE of conventional mice were significantly higher than those in JE of germ‐free mice. Additionally, fluorescent immunohistochemistry showed that S 100 A 8 expression was observed in the JE of both conventional and germ‐free mice, whereas S 100 A 9 was expressed in the JE of conventional but not germ‐free mice. Conclusion S 100 A 8 protein is expressed in JE cells of mice in the presence and in the absence of infection with oral bacteria. S 100 A 9 expression in JE cells in the presence of microflora is significantly increased compared with the absence of microflora, which suggests that S 100 A 9 expression may be induced by infection of microflora. The production of calprotectin in gingival epithelial cells may be mediated through S 100 A 9 induction by bacterial infection.