Elevated expression of IL-17 and IL-12 genes in chronic inflammatory periodontal disease

Honda, Takeshi; Aoki, Y.; Takahashi, Naoki; Maekawa, Tomoki; Nakajima, Takako Eguchi; Ito, H.; Tabeta, Koichi; Okui, Takafumi; Kajita, K.; Domon, Hisanori; Yamazaki, Kazuhisa

doi:10.1016/j.cca.2008.06.003

Cited by 61 publications

(43 citation statements)

References 42 publications

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“…IL-17 is a potent inducer of inflammation and studies have shown it to be involved in autoimmune diseases such as rheumatoid arthritis (40,41). Recent studies have reported that the IL-17 levels in gingival samples are higher in periodontitis patients than healthy patients, indicating that Th17 cells may play a significant role in the inflammatory response associated with chronic periodontitis (12,30,59). Since PAR-2 activation in a variety of cells causes upregulation of IL-6, a potent inducer of Th 17 cell production (11), this pathway could be involved in the upregulation of IL-17 levels seen in the T-cell supernatants from PAR-2 ϩ/ϩ mice and thus the lower levels of IL-17 seen in the PAR2 Ϫ/Ϫ mice may be a consequence of the lower levels of IL-6 observed.…”

Section: Vol 78 2010 Role Of Par-2 In Periodontitis 635mentioning

confidence: 99%

Protease-Activated Receptor 2 Has Pivotal Roles in Cellular Mechanisms Involved in Experimental Periodontitis

et al. 2010

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The tissue destruction seen in chronic periodontitis is commonly accepted to involve extensive upregulation of the host inflammatory response. Protease-activated receptor 2 (PAR-2)-null mice infected with Porphyromonas gingivalis did not display periodontal bone resorption in contrast to wild-type-infected and PAR-1-nullinfected mice. Histological examination of tissues confirmed the lowered bone resorption in PAR-2-null mice and identified a substantial decrease in mast cells infiltrating the periodontal tissues of these mice. T cells from P. gingivalis-infected or immunized PAR-2-null mice proliferated less in response to antigen than those from wild-type animals. CD90 (Thy1.2) expression on CD4؉ and CD8 ؉ T-cell-receptor ␤ (TCR␤) T cells was significantly (P < 0.001) decreased in antigen-immunized PAR-2-null mice compared to sham-immunized PAR-2-null mice; this was not observed in wild-type controls. T cells from infected or antigen-immunized PAR-2-null mice had a significantly different Th1/inflammatory cytokine profile from wild-type cells: in particular, gamma interferon, interleukins (interleukin-2, -3, and -17), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor alpha demonstrated lower expression than wild-type controls. The absence of PAR-2 therefore appears to substantially decrease T-cell activation and the Th1/inflammatory response. Regulation of such proinflammatory mechanisms in T cells and mast cells by PAR-2 suggests a pivotal role in the pathogenesis of the disease.

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Section: Vol 78 2010 Role Of Par-2 In Periodontitis 635mentioning

confidence: 99%

Protease-Activated Receptor 2 Has Pivotal Roles in Cellular Mechanisms Involved in Experimental Periodontitis

et al. 2010

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“…In addition, peripheral blood mononuclear cells from patients with gingivitis and periodontitis stimulated with outer membrane protein of P. gingivalis express IL-17 (Oda et al, 2003). IL-17 mRNA was shown to be expressed in gingival tissue, with higher levels in diseased tissues (Honda et al, 2008;Cardoso et al, 2009). In vitro, IL-17 stimulates HGF to produce IL-6, IL-8, and MMPs (Beklen et al, 2007;Mahanonda et al, 2008).…”

Section: Introduction Imentioning

confidence: 99%

IL-17 in Sera from Patients with Aggressive Periodontitis

Schenkein¹,

Koertge²,

Brooks

et al. 2010

J Dent Res

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Interleukin-17 (IL-17), the prototype cytokine produced by the Th17 subset of T-helper cells, plays a role in inflammatory responses, autoimmunity, and antimicrobial responses in a variety of infectious and inflammatory diseases. In view of the inflammatory nature and severity of aggressive periodontitis, we hypothesized that IL-17 might be detected in sera from patients with aggressive periodontitis. We used ELISA to measure IL-17 serum concentrations from 67 periodontally healthy (NP) individuals and from 53 patients with localized (LAgP) and 49 patients with generalized (GAgP) aggressive periodontitis. IL-17 was barely detectable in sera from periodontally healthy individuals (1.9 ± 2.0 pg/mL), but was present at significantly higher concentrations in sera from those with LAgP (7.6 ± 2.2 pg/mL) and GAgP (17.1 ± 2.3 pg/mL). Multivariate analyses demonstrated associations of IL-17 concentrations with periodontal attachment loss, but not with current smoking. Therefore, Th17 responses may be characteristic of AgP, and IL-17 may play a role in the pathogenesis of aggressive periodontitis.

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“…Prior to the discovery of Th17 cells, it was suggested that Th1 cells are characteristic of a ‘stable’ lesions, whereas Th2 cells are associated with disease (14). However, IL-17 has also been documented in periodontitis patients with severe disease (19–22), and a significant number of CD4 + T cells isolated from gingival tissue of periodontitis patients express IL-17 (23). In P. gingivalis murine infections, IL-17 signaling is host-protective by virtue of limiting infection via neutrophil mobilization (24).…”

Section: Introductionmentioning

confidence: 99%

TLR2 Signaling and Th2 Responses Drive Tannerella forsythia-Induced Periodontal Bone Loss

Myneni

Settem

Connell

et al. 2011

The Journal of Immunology

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Periodontal disease (PD) is a chronic inflammation of the tooth supporting soft tissue and alveolar bone due to infection by a select group of gram negative microbes, and leads to tooth loss if untreated. Since mice deficient in CD4+ cells are resistant to infection-induced alveolar bone loss, Th cells have been implicated in bone destructive processes during PD. However, the extent to which different Th-cell subtypes play roles in pathogenesis or host protection remains to be defined, and is likely to vary depending on the dominant microorganism involved. By far the best studied periodontal microbe in PD is Porphyromonas gingivalis. Even though the gram negative anaerobe Tannerella forsythia is also a vital contributor to periodontal bone loss, almost nothing is known about immune responses to this organism. Previous studies from our laboratory have revealed that T. forsythia induces periodontal bone loss in mice, and that this bone loss depends on the bacterially-expressed BspA protein. In this study, we show that T. forsythia activates murine APCs primarily through TLR2-dependent signaling via BspA. Furthermore, T. forsythia infection causes a pronounced Th2 bias, evidenced by T cell expression of IL-5 but not IFN-γ or IL-17 in draining LN. Consistently, deficiencies in TLR2 or STAT6 result in resistance to T. forsythia-induced alveolar bone loss. Thus, TLR2 signaling and Th2 cells play pathogenic roles in T. forsythia-induced alveolar bone destruction.

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Elevated expression of IL-17 and IL-12 genes in chronic inflammatory periodontal disease

Cited by 61 publications

References 42 publications

Protease-Activated Receptor 2 Has Pivotal Roles in Cellular Mechanisms Involved in Experimental Periodontitis

Protease-Activated Receptor 2 Has Pivotal Roles in Cellular Mechanisms Involved in Experimental Periodontitis

IL-17 in Sera from Patients with Aggressive Periodontitis

TLR2 Signaling and Th2 Responses Drive Tannerella forsythia-Induced Periodontal Bone Loss

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