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We have previously shown that Foxp3 CD4 regulatory T (Foxp3 Treg) cells are elevated in inflamed gingival tissues of mice infected with Porphylomonas gingivalis (P. gingivalis), a major periopathologic bacteria. Foxp3 Treg cells play a crucial role in maintaining immune tolerance and homeostasis. In this study, we elucidated the mechanisms of Foxp3 Treg cell induction at sites of inflamed gingival tissue. A murine periodontal disease model with alveolar bone loss was established by oral infection with 10 cfu of P. gingivalis suspended in 0.1ml of PBS with 2% carboxymethylcellulose, 15 times over three weeks. Gingival mononuclear cells were isolated from mouse gingival tissues for analysis by kinetic observation. Elevated numbers of CD11c dendritic cells (DCs) but low expression of co-stimulatory (CD40, 80, 86) and MHC-II were detected in inflamed gingival tissues. Interestingly, significantly induction of IL-6 and TGF-β transcripts was detected in early stages of the inflammation period. Furthermore, expression levels of TGF-β transcripts were maintained through the end of experiment. Importantly, diminished levels of IL-6 transcripts but significant induction of retinal dehydrogenase 2 (RALDH2) transcripts, a major enzyme for retinoic acid synthesis, were detected in later stages of the inflammation period. These results suggest that inflammation-derived CD11c DCs regulate inflammation and induce Foxp3 Treg cells in the gingiva of the mouse model.

Characterization of Inflammation-derived CD11c+ Dendritic Cells in Mouse Model of Periodontal Disease