Cytokine Expression in Periodontal Health and Disease

Okada, Hiroshi; Murakami, Shinya

doi:10.1177/10454411980090030101

Cited by 505 publications

(543 citation statements)

References 154 publications

(120 reference statements)

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“…IL-6 has an ability to induce osteoclastogenesis 15) and IL-8 acts as a chemoattractant for neutrophils (reviewed in ref. 16). Therefore, these cytokines are closely associated with onset of periodontal disease.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

Ara

Maeda

Fujinami

et al. 2008

Biological & Pharmaceutical Bulletin

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In the present study, we investigated the anti-inflammatory effects of a Kampo medicine Shosaikoto (TJ-9) using in vitro periodontal disease model, in which human gingival fibroblasts (HGFs) treated with lipopolysaccharide (LPS) from Porphyromonas gingivalis (PgLPS) produce IL-6, IL-8 and prostaglandin E 2 (PGE 2 ). Treatment with PgLPS (10 ng/ml), TJ-9 (up to 1 mg/ml) and their combinations for 24 h did not affect the viability of HGFs. Moreover, TJ-9 did not alter LPS-induced IL-6 and IL-8 productions. However, TJ-9 significantly suppressed LPS-induced PGE 2 production in a dose-dependent manner but TJ-9 alone did not affect basal PGE 2 level. Western blotting demonstrated that TJ-9 decreased cyclooxygenase-2 (COX-2) expression in a dosedependent manner but not phospholipase A 2 . Moreover, TJ-9 selectively and dose-dependently inhibited COX-2 activity. These results suggest that TJ-9 decreased PGE 2 production by inhibition of both COX-2 expression and activity and that TJ-9 may be useful to improve gingival inflammation in periodontal disease.

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Section: Discussionmentioning

confidence: 99%

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

Ara

Maeda

Fujinami

et al. 2008

Biological & Pharmaceutical Bulletin

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“…Previously, many researchers have shown the effects of inflammatory cytokines such as IL-1 and IL-6 on periodontal cells, e.g. fibroblasts, epithelial cells and macrophages (20). In periodontal inflamed tissues, IL-1 and IL-6 may be responsible to the tissue destruction by increasing matrix-metalloproteinases (MMPs) (2,20).…”

Section: Methodsmentioning

confidence: 99%

Enhancement of gingival inflammation induced by synergism of IL-1^|^beta; and IL-6

et al. 2013

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Internleukin-1 (IL-1) and IL-6 are the most potent proinflammatory cytokines being involved in inflammatory diseases such as periodontitis. The objective of this study was to examine the synergistic effects of IL-1β and IL-6 on gingival inflammation by targeting cultured human gingival fibroblasts (HGFs). HGFs were treated with IL-1β or IL-6/soluble IL-6R (sIL-6R), and total RNA and total cell lysate were collected to examine expression of gp130 known as a signal transducer of IL-6 using qRT-PCR and Western blotting. IL-1β-mediated IL-6 productivity in HGFs was examined using ELISA method. Likewise, after HGFs and THP-1 macrophages were treated with IL-1β, TNF-α and IL-6, sIL-6R productivity was examined. Next, HGFs were treated with IL-6/ sIL-6R after pretreatment of IL-1β, and the intracellular signals were examined using Western blotting. Finally, various mRNA/protein expressions in HGFs treated with IL-6/sIL-6R after pretreatment of IL-1β were examined using qRT-PCR and ELISA method. IL-1β increased significantly both gp130 and IL-6 expression in HGFs. IL-6 increased significantly sIL-6R production in THP-1 macrophages but not HGFs. Co-stimulation with IL-1β and IL-6/sIL-6R induced dramatically the phosphorylation of Stat3, ERK and JNK in HGFs. Interestingly, expression of various inflammation-related molecules such as MMP-1, MCP-1, IL-1ra, bFGF and VEGF were enhanced by co-stimulation with IL-1β and IL-6/sIL-6R in HGFs. Gingival inflammation is regulated by HGFs affected by both IL-1β and IL-6/sIL-6R synergistically through induction of gp130 expression, resulting in progression of periodontitis.

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“…Actúan regulando las células endoteliales y las moléculas de adhesión leucocitarias, hecho imprescindible para que los leucocitos abandonen los vasos sanguíneos y se infiltren en los tejidos circundantes. En tejidos clínicamente sanos, se ha observado la presencia en baja cantidad de citoquinas proinflamatorias como IL-1ß, IL-6 y TNF-α, ya que la concentración de citoquinas debe ser adecuada para mantener la homeostasis de los tejidos 4 (Fig. 1).…”

Section: Resumen Resumen Resumen Resumenunclassified

<A NAME="top"></A>Papel de la IL-6 y TNF-alfa en la enfermedad periodontal

Sainz

Kass²,

Martínez³

2006

Avances en Periodoncia

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Cytokine Expression in Periodontal Health and Disease

Abstract: Soluble proteins that serve as mediators of cell function and are produced by various cell types, such as structural and inflammatory cells, are collectively called cytokines.

Cited by 505 publications

References 154 publications

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

Preventive Effects of a Kampo Medicine, Shosaikoto, on Inflammatory Responses in LPS-Treated Human Gingival Fibroblasts

Enhancement of gingival inflammation induced by synergism of IL-1^|^beta; and IL-6

<A NAME="top"></A>Papel de la IL-6 y TNF-alfa en la enfermedad periodontal

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