Porphyromonas gingivalis antigen preferentially stimulates T cells to express IL-17 but not receptor activator of NF-kappaB ligand in vitro.
Although T cells have been implicated in the pathogenesis and are considered to be central to both their progression and control of chronic inflammatory periodontal diseases, the precise contribution of T cells to tissue destruction has not been fully clarified. Recently, interleukin (IL)-17 and receptor activator of Nuclear factor kappaB NF-kappaB ligand (RANKL) have received much attention as a result of their proinflammatory and bone metabolic roles, respectively. We therefore investigated the effect of outer membrane protein (OMP) from Porphyromonas gingivalis (P. gingivalis) on the expression of IL-17 and RANKL in peripheral blood mononuclear cells (PBMCs) and compared these between gingivitis and periodontitis, which are representative of stable and progressive lesions, respectively. The in situ expression of these molecules was also examined. P. gingivalis OMP stimulated PBMCs to express IL-17 at both the mRNA and protein level. Although the mean expression of mRNA was not different between the two groups, the mean level of IL-17 in the culture supernatants was higher in gingivitis patients than in periodontitis patients. However, the frequency of IL-17-positive samples was higher in the periodontitis patients. This stimulatory effect was not evident for RANKL expression in either periodontitis or gingivitis patients. In gingival tissue samples, IL-17 mRNA was detected in gingivitis more frequently than in periodontitis. The expression of RANKL mRNA was much lower than that of IL-17 in terms of both level and frequency. These results suggest that IL-17 but not RANKL may be involved in the pathogenesis of periodontal diseases. However, there may be negative regulatory mechanisms for IL-17 in gingivitis.
Oda
T
T
Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yoshie
H
H
Yamazaki
K
K
D000328:Adult; D000368:Aged; D000942:Antigens, Bacterial / Q000502:physiology; D001425:Bacterial Outer Membrane Proteins / Q000502:physiology; D005434:Flow Cytometry; D005891:Gingivitis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D008875:Middle Aged; D010518:Periodontitis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000276:immunology* / Q000472:pathogenicity; D012333:RNA, Messenger / Q000096:biosynthesis; D053246:Receptor Activator of Nuclear Factor-kappa B; D018124:Receptors, Tumor Necrosis Factor / Q000096:biosynthesis*; D018709:Statistics, Nonparametric; D013601:T-Lymphocytes / Q000378:metabolism* / Q000382:microbiology
D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D020381:Interleukin-17; D012333:RNA, Messenger; D053246:Receptor Activator of Nuclear Factor-kappa B; D018124:Receptors, Tumor Necrosis Factor