Cytokine profiles of cells extracted from humans with periodontal diseases.
FACS analysis was used to determine the percent interferon (IFN)-gamma-, interleukin (IL)-4-, IL-10-, and CD30-positive T-cells extracted from adult periodontitis (AP) and healthy/gingivitis (H/G) subjects. Additionally, the percentages of IL-1 beta-, IL-10- and IL-12-producing B-cells and macrophages were ascertained. The percent IL-10+ CD8 cells extracted from AP lesions was decreased compared with H/G tissues (p = 0.033), and the percent CD30+ CD4 (p = 0.001) and CD30+ CD8 (p = 0.028) cells was higher in AP than in H/G tissues. The percentages of IL-1 beta + macrophages (p = 0.003) and IL-12+ B-cells (p = 0.034) were both higher in AP lesions than in H/G tissues. The specific effect of Porphyromonas gingivalis on the cytokine profiles of peripheral blood mononuclear cells isolated from P. gingivalis-infected AP and H/G patients was also determined. While there were no significant differences in the percent cytokine-positive T-cells after stimulation with P. gingivalis outer membrane antigens (OM) for 6 days compared with cells incubated in medium only, the percent CD30+ CD4 cells increased significantly (p = 0.047 and p = 0.063 for AP and H/G groups, respectively). There was also an increase in the percent IL-1 beta + B-cells from AP patients (p = 0.029), and the percent IL-12+ monocytes from AP and H/G subjects was higher than the percent IL-12+ B-cells, both after stimulation with P. gingivalis OM (p = 0.005 for the AP group and p = 0.058 and therefore not quite significant for the H/G group) and when incubated in medium alone (p = 0.016 and p = 0.015 for AP and H/G groups, respectively). This study has shown that IL-10+ CD8 cells may be significant in gingival lesions, and that CD30+ T-cells indicative of Th2 or Th0 cells may play a role in progressive periodontal disease. This study has also shown that B-cells produce IL-1 in the gingival lesion and that P. gingivalis may be significant in the induction of B-cell-induced IL-1.
Gemmell
E
E
Department of Dentistry, University of Queensland, Australia.
Seymour
G J
GJ
D000328:Adult; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000032:analysis*; D018450:Disease Progression; D005260:Female; D005891:Gingivitis / Q000097:blood / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D006801:Humans; D007371:Interferon-gamma / Q000032:analysis; D007375:Interleukin-1 / Q000032:analysis; D016753:Interleukin-10 / Q000032:analysis; D018664:Interleukin-12 / Q000032:analysis; D015847:Interleukin-4 / Q000032:analysis; D017730:Ki-1 Antigen / Q000032:analysis; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D010518:Periodontitis / Q000097:blood / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D010519:Periodontium / Q000276:immunology / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D001425:Bacterial Outer Membrane Proteins; D016207:Cytokines; D007375:Interleukin-1; D017730:Ki-1 Antigen; D016753:Interleukin-10; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma