Expression profile of macrophage migration inhibitory factor in periodontitis

Objective: Macrophage migration inhibitory factor (MIF) is a pivotal mediator of host innate immunity and influences the development of several inflammatory diseases. The role of MIF in periodontitis is unclear. Methods: Eighteen periodontally healthy volunteers and 18 patients with stage III or IV periodontitis were enrolled. Blood samples and gingival tissues were collected from all individuals. The serum concentrations of MIF and MCP-1 were measured by ELISA. The protein and mRNA levels of MIF and MCP-1 in gingival tissue were evaluated by immunohistochemical staining and quantitative PCR. The levels of secreted MIF and MCP-1, as well as their mRNA levels, were determined by ELISA and quantitative PCR in oral epithelial cells infected with Porphyromonas gingivalis. Results: After adjusting for age, the level of MCP-1 was significantly higher in the serum and gingival tissue of periodontitis patients, as well as in infected epithelial cells. The serum concentration of MIF was increased in periodontitis patients (15.25 +/- 2.16 ng/mL, P < 0.05) compared to healthy controls (10.43 +/- 1.02 ng/mL). Increased MIF immunoreactivity was found in gingival epithelial tissue but not in the gingival connective tissue of periodontitis patients. The secretion of MIF was 3.82-fold higher in the supernatant of infected cells than in the supernatant of control (P < 0.01). No increase in the MIF mRNA level was found in either gingival tissue or epithelial cells. Conclusions: Based on our limited evidence, we showed the level of MIF was related to periodontal conditions. P. gingivalis may contribute to the development and progression of periodontitis through MIF.

Automated summary

This study revealed significant increases in levels of MCP-1 and MIF in periodontitis patients, along with enhanced secretion of MIF in gingival epithelial tissue. Limited evidence suggested a correlation between MIF and periodontal conditions, with Porphyromonas gingivalis potentially contributing to periodontitis development and progression through MIF.