Neonatal-Fc-Receptor-Mediated Transport of Bacterial Immune Complex into Periodontal Tissue

OBJECTIVES: Elevated IgG-antibody to periodontal bacteria is a characteristic of periodontitis. However, it is unclear by what route and mechanism bacterial antigens are delivered from oral cavity to the lamina propria. Recently, the neonatal-Fc-receptor (FcRn) was identified as a transporter of bacterial-IgG-immune complexes (IC) from lumen to subepithelial tissue of the intestine. Based on this, the objectives of the present study were to determine the expression profile of FcRn in gingival epithelium and to examine the role of FcRn in the transportation of bacterial-IgG-IC to gingival lamina propria.

METHODS: The expression of FcRn-mRNA and FcRn-protein in rat and human gingival epithelial cells (GEC) was evaluated by RT-PCR and immunohistochemical (IHC) staining, respectively. The IC used in this study was formed in vitro between Omp29, outer-membrane protein of Aggregatibacter actinomycetemcomitans (Aa), and specific polyclonal IgG-antibody to Aa. To examine in vivo if IC transportation from oral cavity to gingival lamina propria occurs, periodontitis rat models were used. FcRn-KO and wild type mice were also employed for in vivo IC transportation assay. Transposed IC in the gingival tissue homogenates were quantitated by a modified ELISA system using C1q complement as the IC detection module.

RESULTS: FcRn-mRNA was present in both human and rat GEC. FcRn expression was induced by stimulation with periodontopathogenic bacteria. According to IHC staining, the production of FcRn in inflamed tissue was higher than that found in normal healthy tissue of both human and rats. Animal in vivo models revealed that FcRn can transport orally applied IC to gingival lamina propria in an inflammation-prone manner.

CONCLUSION: FcRn expressed in gingival epithelium can transpose bacterial antigen in the form of IC to gingival laminar propria, suggesting that gingival epithelial cells facilitate an antigen transport mechanism based on their expression of FcRn.

Supported by IADR-GSK and NIDCR DE18310.