Interleukin‐18 Concentrations and the Pathogenesis of Periodontal Disease

Johnson, Roger B.; Serio, Francis G.

doi:10.1902/jop.2005.76.5.785

Cited by 70 publications

(81 citation statements)

References 34 publications

(55 reference statements)

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“…The ability of a CR3 antagonist (XVA143) to reverse suppression of IL-12p70, and thereby negate these immune evasion effects, holds promise for a potential therapeutic immunomodulation in human periodontitis and perhaps associated systemic diseases. Our results and their interpretation are in line with clinical research studies indicating an inverse relationship between IL-12p70 and severity of periodontitis, concluding that periodontal infection and resulting inflammation may perpetuate due to decreased IL-12p70 levels (41,42,62).…”

Section: Discussionsupporting

confidence: 91%

Complement Receptor 3 Blockade Promotes IL-12-Mediated Clearance of Porphyromonas gingivalis and Negates Its Virulence In Vivo

Hajishengallis

Shakhatreh²,

Wang³

et al. 2007

The Journal of Immunology

112

158

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The ability of certain pathogens to exploit innate immune function allows them to undermine immune clearance and thereby increase their persistence and capacity to cause disease. Porphyromonas gingivalis is a major pathogen in periodontal disease and is associated with increased risk of systemic conditions. We have previously shown that the fimbriae of P. gingivalis interact with complement receptor 3 (CR3; CD11b/CD18) in monocytes/macrophages, resulting in inhibition of IL-12p70 production in vitro. The in vivo biological implications of this observation were investigated in this study using a CR3 antagonist (XVA143). XVA143 was shown to block CR3 binding of P. gingivalis fimbriae and reverse IL-12p70 inhibition; specifically, CR3 blockade resulted in inhibition of ERK1/2 phosphorylation and up-regulation of IL-12 p35 and p40 mRNA expression. Importantly, mice pretreated with XVA143 elicited higher IL-12p70 and IFN-γ levels in response to P. gingivalis i.p. infection and displayed enhanced pathogen clearance, compared with similarly infected controls. The notion that CR3 is associated with reduced IL-12p70 induction and impaired P. gingivalis clearance was confirmed using i.p. infected wild-type and CR3-deficient mice. Moreover, XVA143 dramatically attenuated the persistence and virulence of P. gingivalis in experimental mouse periodontitis, as evidenced by reduced induction of periodontal bone loss. Therefore, CR3 blockade may represent a promising immunomodulatory approach for controlling human periodontitis and possibly associated systemic diseases.

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Section: Discussionsupporting

confidence: 91%

Complement Receptor 3 Blockade Promotes IL-12-Mediated Clearance of Porphyromonas gingivalis and Negates Its Virulence In Vivo

Hajishengallis

Shakhatreh²,

Wang³

et al. 2007

The Journal of Immunology

112

158

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“…1,3 The ILs are a group of cytokines that have complex immunological roles including proliferation, migration, growth, and differentiation of cells. 4,6 Interleukin-18 is a proinflammatory cytokine and associate of the IL-1 family that has the ability to encourage either Th1 or Th2 cells in reaction to Gram-negative infections. 8 It has only been scrutinized in a small number of studies to date, looking at different loci.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have stated the connotation between IL-18 and the pathogenesis of periodontal disease. 6,7 Further, they stated that IL-18 concentration was higher in periodontal sites where the probing depth was > 6 mm when compared with healthy sites. Interleukin-18 is primarily formed by oral epithelial cells, osteoblasts, adrenal cortex cells, and antigen-presenting cells.…”

Section: 5005/jp-journals-10024-2180mentioning

confidence: 99%

Effect of Periodontal Therapy on Crevicular Fluid Interleukin-18 Level in Periodontal Health and Disease in Central Maharashtra (India) Population

Mahajani¹,

Jadhao

Wankhade³

et al. 2017

The Journal of Contemporary Dental Practice

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Aim:The incidence and progression of the periodontal disease depend on periodontal microflora and the multifaceted response of the host, and these interactions are mediated by cytokines and chemokines. Interleukin-18 (IL-18) is a proinflammatory cytokine of the IL-1 superfamily. The aim of the present study was the assessment of the periodontal therapy in IL-18 level in periodontal disease and health. Materials and methods:Based on clinical attachment loss (CAL), probing pocket depth (PPD), gingival index (GI), and plaque index (PI) patients were divided into three groups: Group I with healthy patients, group II with chronic periodontitis, and group III with posttreatment patients having periodontitis.Results: Mean PI, PPD, CAL, and gingival crevicular fluid (GCF) volume were significantly higher in groups II and III compared with group I. However, there were no significant differences between GI in groups I, II, and III. The total amount of IL-18 in

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“…Similarly, serum IL-18 was significantly elevated in patients with chronic periodontitis relative to that in healthy subjects (Sánchez-Hernández et al 2011), and increases in IL-18 in gingival biopsy tissues were correlated directly with pocket depth (Johnson and Serio 2005). Thus, several studies have shown that the levels of IL-18 in patients with periodontitis differ from those in healthy subjects.…”

Section: Introductionmentioning

confidence: 95%

Increased Interleukin-18 in the Gingival Tissues Evokes Chronic Periodontitis after Bacterial Infection

Yoshinaka

Shoji

Nishioka

et al. 2014

Tohoku J. Exp. Med.

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Periodontal disease is a chronic inflammatory disease that results in the breakdown of the tooth-supporting tissues, and can ultimately lead to resorption of the alveolar bone. Recently, several studies have shown a close relationship between increased interleukin-18 (IL-18) levels and the pathogenesis of chronic periodontitis, a major cause of tooth loss. However, it has yet to be shown whether chronic periodontitis results from or causes an increase in IL-18 after bacterial infection. In the present study, we investigated how IL-18 overexpression relates to periodontal disease using IL-18 transgenic (Tg) mice. IL-18Tg and wild-type mice were inoculated intraorally with Porphyromonas (P.) gingivalis, which has been implicated in the etiology of chronic periodontitis. Seventy days after P. gingivalis infection, alveolar bone loss and gingival cytokine levels were assessed using histo-morphological analysis and enzyme-linked immunoabsorbent assay, respectively. Periodontal bone loss was evoked in IL-18Tg mice, but not in wild-type mice. Interestingly, levels of bone-resorptive cytokines, including IL-1α, IL-1β, tumor necrosis factor-α, and IL-6, were unchanged in the gingival tissues of IL-18Tg mice infected with P. gingivalis, although levels of interferon γ (a proinflammatory T-helper 1 cytokine) decreased. RT-PCR analysis showed elevated expression of mRNAs for receptor activator of nuclear factor kappa-B ligand (a key stimulator of osteoclast development and activation) and CD40 ligand (a marker of T cell activation) in the gingiva of IL-18Tg mice infected with P. gingivalis. We conclude that increased IL-18 in the gingival tissues evokes chronic periodontitis after bacterial infection, presumably via a T cell-mediated pathway.

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Interleukin‐18 Concentrations and the Pathogenesis of Periodontal Disease

Cited by 70 publications

References 34 publications

Complement Receptor 3 Blockade Promotes IL-12-Mediated Clearance of Porphyromonas gingivalis and Negates Its Virulence In Vivo

Complement Receptor 3 Blockade Promotes IL-12-Mediated Clearance of Porphyromonas gingivalis and Negates Its Virulence In Vivo

Effect of Periodontal Therapy on Crevicular Fluid Interleukin-18 Level in Periodontal Health and Disease in Central Maharashtra (India) Population

Increased Interleukin-18 in the Gingival Tissues Evokes Chronic Periodontitis after Bacterial Infection

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