Assessment of Interleukin‐6 in the Pathogenesis of Periodontal Disease

Takahashi, Keiso; Takashiba, Shogo; Nagai, Atsushi; Takigawa, Morikuni; Myoukai, Fumio; Kurihara, Hidemi; Murayama, Yoji

doi:10.1902/jop.1994.65.2.147

Cited by 157 publications

(131 citation statements)

References 27 publications

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“…The diseased gingiva of periodontitis patients contained higher levels of IL-6, which is capable of stimulating bone resorption (19). However, IL-6 secretion was upregulated by P. gingivalis LPS, the presence of escin reduced IL-6 secretion in hPDLs, indicating that escin may prevent periodontal tissue destruction, including alveolar bone resorption.…”

Section: Discussionmentioning

confidence: 98%

Escin inhibits lipopolysaccharide-induced inflammation in human periodontal ligament cells

Liu

Wang

Qiu

et al. 2012

Molecular Medicine Reports

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Abstract. Periodontitis is a chronic inflammatory disease associated with gram-negative subgingival microflora infection. Accumulating experimental evidence suggests that escin exerts anti-inflammatory and anti-edematous effects. This study was designed to investigate the in vitro effects of escin on the inflammatory reaction of human periodontal ligament cells (hPDLs). hPDLs were stimulated with lipopolysaccharide (LPS). The cells were treated with various concentrations of escin. The viability of hPDLs was evaluated using the MTT method. The expression of Toll-like receptor 2 (TLR2) in hPDLs and the levels of IL-1β, TNF-α and IL-6 in the supernatant were measured. Escin significantly attenuated LPS-induced cytotoxicity in a concentration-dependent manner in hPDLs. Treatment with escin partly blocked the expression of TLR2. Escin also lowered the increase of proinflammatory cytokines (IL-1β, TNF-α and IL-6) induced by LPS. The present findings show that escin exerts a protective effect against LPS-induced inflammation in hPDLs. It was also shown that escin is a promising medicine for the treatment of periodontitis.

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Section: Discussionmentioning

confidence: 98%

Escin inhibits lipopolysaccharide-induced inflammation in human periodontal ligament cells

Liu

Wang

Qiu

et al. 2012

Molecular Medicine Reports

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“…In the majority of investigations carried out, IL-6 expression was found to be higher at sites of periodontal inflammation (20). IL-6 levels were found to be increased in diseased gingiva from patients with periodontitis compared to gingiva from periodontally healthy subjects (5,52). Compared to normal tissue, IL-6 expression appears to be elevated in inflamed tissue from periodontitis sites and is highest in gingivitis sites (33,59).…”

Section: Discussionmentioning

confidence: 99%

Arginine-Specific Protease fromPorphyromonas gingivalisActivates Protease-Activated Receptors on Human Oral Epithelial Cells and Induces Interleukin-6 Secretion

et al. 2001

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Periodontitis is a chronic inflammatory disease affecting oral tissues. Oral epithelial cells represent the primary barrier against bacteria causing the disease. We examined the responses of such cells to an argininespecific cysteine proteinase (RgpB) produced by a causative agent of periodontal disease, Porphyromonas gingivalis. This protease caused an intracellular calcium transient in an oral epithelial cell line (KB), which was dependent on its enzymatic activity. Since protease-activated receptors (PARs) might mediate such signaling, reverse transcription-PCR was used to characterize the range of these receptors expressed in the KB cells. The cells were found to express PAR-1, PAR-2, and PAR-3, but not PAR-4. In immunohistochemical studies, human gingival epithelial cells were found to express PAR-1, PAR-2, and PAR-3 on their surface, but not PAR-4, indicating that the cell line was an effective model for the in vivo situation. PAR-1 and PAR-2 expression was confirmed in intracellular calcium mobilization assays by treatment of the cells with the relevant receptor agonist peptides. Desensitization experiments strongly indicated that signaling of the effects of RgpB was occurring through PAR-1 and PAR-2. Studies with cells individually transfected with each of these two receptors confirmed that they were both activated by RgpB. Finally, it was shown that, in the oral epithelial cell line, PAR activation by the bacterial protease-stimulated secretion of interleukin-6. This induction of a powerful proinflammatory cytokine suggests a mechanism whereby cysteine proteases from P. gingivalis might mediate inflammatory events associated with periodontal disease on first contact with a primary barrier of cells.

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“…Finally, local vs. systemic cytokine profiles differ substantially in patients with periodontal disease. It therefore appears that regulation of Tcell activity in periodontal disease occurs locally, and these changes may not be manifested systemically (Fujihashi et al, 1993;Takahashi et al, 1994;Prabhu et al, 1996 (Taubman et al, 1994;Prabhu et al, 1996) indeed demonstrates the presence of Thl cells in GMC. In contrast, if a Th2 response (characterized by IL-4, IL-5, and IL-10 production) predominates, the cellular infiltrate would be characterized by increased B-cell development and increased antibody production.…”

Section: A) Proliferative Responses Of Peripheral Blood (Pb) T-lymphomentioning

confidence: 99%

Cell-Mediated Immune System Regulation in Periodontal Diseases

Mathur

Michalowicz

1997

Critical Reviews in Oral Biology & Medicine

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The adaptive immune system consists of humoral and cell-mediated immunity. T-lymphocytes are the key components of cell-mediated immunity. CD4+ helper T-lymphocytes facilitate B-cells to differentiate and produce specific antibodies, whereas CD8+ cytotoxic T-lymphocytes kill virally infected cells. Periodontal diseases have been associated with a variety of imbalances in the regulation of immune responses. Changes in the ratios of peripheral blood CD4+ and CD8+ T-lymphocytes, depressed proliferative responses of peripheral blood lymphocytes, and increased frequency of CD45RO+ memory T-lymphocytes in diseased tissues have been reported in individuals with various forms of periodontal disease. While some studies have shown an increased frequency of 'y+ T-cells in periodontal lesions, the role of y8+ T-cells in periodontal disease remains controversial. The ability of putative periodontopathic bacteria selectively to stimulate certain VP3-expressing T-cells is intriguing and could determine whether a CD4+ Th 1 or a CD4+ Th2 cell response is elicited. The prominence of a particular subset of helper T-cells within the periodontal lesion could be a reflection of the stage and activity of the disease, or the types of bacteria present. Regardless, longitudinal studies of the involvement of T-cell subsets and cytokines in periodontal disease are clearly needed.

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Assessment of Interleukin‐6 in the Pathogenesis of Periodontal Disease

Cited by 157 publications

References 27 publications

Escin inhibits lipopolysaccharide-induced inflammation in human periodontal ligament cells

Escin inhibits lipopolysaccharide-induced inflammation in human periodontal ligament cells

Arginine-Specific Protease fromPorphyromonas gingivalisActivates Protease-Activated Receptors on Human Oral Epithelial Cells and Induces Interleukin-6 Secretion

Cell-Mediated Immune System Regulation in Periodontal Diseases

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