title: Induction of IL-10-producing CD4+ T-cells in chronic periodontitis.
abstract: Precise immunological aspects of inflamed gingival mucosa remain to be elucidated in the murine experimental periodontitis model; therefore, we have characterized the mucosal immune cells in the inflamed gingiva of mice with alveolar bone reduction. Mice were orally infected with Porphyromonas gingivalis 15 times over 2 weeks. Gingival mononuclear cells (GMCs) were isolated from P. gingivalis- and sham-infected mice 1, 7, 15, and 30 days after the last infection. Although the greatest degree of periodontitis was seen in P. gingivalis-infected mice at 30 days after infection, the highest levels of IL-6 and TNF-α production were noted in the GMCs isolated 7 days after infection. Further, the frequency of RANKL(+)CD4(+) T-cells in GMCs of inflamed gingiva peaked 15 days after infection. Importantly, the number of Foxp3(+)CD4(+) CD25(+) regulatory T (Treg)-cells was increased only in the experimental group 30 days after infection. Thus, intracellular cytokine analysis revealed an increased number of IL-10-producing CD4(+) T-cells in inflamed gingiva when compared with the control group. These results suggest that there are potential roles for Treg cells during the chronic stage of periodontitis in the regulation of gingival inflammation and alveolar bone loss.
authors.affiliation: Department of Pediatric Dentistry, Immunobiology Vaccine Center, Institute of Oral Health Research, School of Dentistry, University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA.
authors.forename: R
authors.initials: R
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Kono
authors.forename: B A
authors.initials: BA
authors.lastname: Bolerjack
authors.forename: Y
authors.initials: Y
authors.lastname: Fukuyama
authors.forename: R S
authors.initials: RS
authors.lastname: Gilbert
authors.forename: K
authors.initials: K
authors.lastname: Fujihashi
authors.forename: J
authors.initials: J
authors.lastname: Ruby
authors.forename: K
authors.initials: K
authors.lastname: Kataoka
authors.forename: M
authors.initials: M
authors.lastname: Wada
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: K
authors.initials: K
authors.lastname: Fujihashi
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology / Q000276:immunology* / Q000382:microbiology; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism; D055113:Chronic Periodontitis / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D005891:Gingivitis / Q000276:immunology / Q000382:microbiology; D018836:Inflammation Mediators / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis*; D015850:Interleukin-6 / Q000096:biosynthesis; D051379:Mice; D008807:Mice, Inbred BALB C; D009061:Mouth Mucosa / Q000276:immunology; D016966:Porphyromonas gingivalis; D053245:RANK Ligand / Q000096:biosynthesis; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D018836:Inflammation Mediators; D015850:Interleukin-6; D053245:RANK Ligand; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10