Involvement of CD14 on human gingival fibroblasts in Porphyromonas gingivalis lipopolysaccharide-mediated interleukin-6 secretion

Wang, Pao-Li; Sato, Katsuaki; Oido, Mari; Fujii, Takeo; Kowashi, Yusuke; Shinohara, Mitsuko; Ohura, Kiyoshi; Tani, Hiroshi; Kuboki, Yoshinori

doi:10.1016/s0003-9969(98)00056-9

Cited by 60 publications

(76 citation statements)

References 30 publications

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“…Cells HGFs were prepared from explants of human normal gingival tissues as described previously, 14) and were maintained in culture medium in a humidified atmosphere of 5% CO 2 at 37°C. HGFs were used between 10th to 20th passages in the assays.…”

Section: Methodsmentioning

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: Methodsmentioning

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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“…Cell culture HGF cells were obtained according to the literature 21) . The HGFs were cultured in Dulbecco's Modified Eagle Medium (DMEM, Nissui Pharmaceutical Co., Ltd., Tokyo, Japan) with 10% fetal bovine serum (FBS), 100 units/ml penicillin G, and 100 g/ml streptomycin at 37ºC in an incubator with 5% CO 2 and 95% humidified air 22) .…”

Section: Reagentsmentioning

confidence: 99%

“…For MTT assay, the cells were cultured with Melsmon at 150 g/ml, 1500 g/ml, 15000 g/ml in DMEM containing 10% FBS (10% DMEM) for 24 h. The subsequent procedures were performed as described elsewhere 21) .…”

Section: Mtt Assaymentioning

confidence: 99%

Evaluation of Collagen Type-1 Production and Anti-Inflammatory Activities of Human Placental Extracts in Human Gingival Fibroblasts

Akagi¹,

Imamura

Makita

et al. 2016

J. Hard Tissue Biology.

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Placental extracts contain various bioactive agents and are thought to be a prospective medicine for oral diseases. However, detailed information regarding their mechanisms with respect to treatment of periodontal diseases is not available, thereby hindering their reliable application in dentistry. In this study, we demonstrated that human placental extracts increased collagen type-1 production, which is linked to the regenerative capabilities of periodontal tissue, on primary human gingival fibroblasts in vitro. Generally, deterioration of periodontal tissue occurs when various types of cytokines are released by periodontal tissue cells in response to stimulation by plaque. However, we exhibited that human placental extracts hindered the pro-inflammatory cytokines such as interleukin (IL)-6 and IL-8 secretion from primary human gingival fibroblasts in vitro. The results contribute to understanding a therapeutic mechanism underlying the effect of human placenta extracts against periodontal disease by modulating the function of human gingival fibroblasts.

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“…Among these pathways are the mitogen-activated protein kinases (MAPKs), which are a highly conserved family of protein serine/threonine kinases and include the extracellular signal-regulated kinases ERK-1 and ERK-2 (11,12). Along with nuclear factor-B (NF-B) activation, ERK activation is often used as a hallmark of LPSinduced signal transduction in many cell types (13)(14)(15)(16)(17)(18)(19). It has been proposed that ERK (p42/p44 MAPK) activation is involved in LPS-induced cellular responses, such as the increased production of TNF␣, inducible nitric-oxide synthase (iNOS) and NO, and interleukin-6 (IL-6) (20 -22).…”

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confidence: 99%

A Differential Role for the Mitogen-activated Protein Kinases in Lipopolysaccharide Signaling

Watters¹,

Sommer²,

Pfeiffer³

et al. 2002

Journal of Biological Chemistry

116

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Endotoxin (lipopolysaccharide, LPS) is a component of the outer membrane of Gram-negative bacteria and promotes the activation of macrophages and microglia. Although these cells are highly LPS-responsive, they serve unique tissue-specific functions and exhibit different LPS sensitivities. Accordingly, it was of interest to evaluate whether these biological differences reside in variations within LPS signaling pathways between these two cell types. Because the mitogen-activated protein kinases ERK-1 and ERK-2 have been implicated in the control of many immune responses, we tested the concept that they are a key indicator for differences in cellular LPS sensitivity. We observed that murine RAW 264.7 macrophages and murine BV-2 microglial cells both respond to LPS by exhibiting increased IB␣ degradation, enhanced NF-B DNA binding activity, and elevated nitric oxide and interleukin-1␤ production. Although LPS potently stimulates ERK activation in RAW 264.7 macrophages, it does not activate ERK-1/-2 in BV-2 microglia. Moreover, antagonism of the MEK/ERK pathway potentiates LPS-stimulated nitric oxide production, suggesting that LPS-stimulated ERK activation can exert inhibitory effects in macrophage-like cells. These data support the idea that ERK activation is not a required function of LPS-mediated signaling events and illustrate that alternative/additional pathways for LPS action exist in these cell types.

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Involvement of CD14 on human gingival fibroblasts in Porphyromonas gingivalis lipopolysaccharide-mediated interleukin-6 secretion

Cited by 60 publications

References 30 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

Evaluation of Collagen Type-1 Production and Anti-Inflammatory Activities of Human Placental Extracts in Human Gingival Fibroblasts

A Differential Role for the Mitogen-activated Protein Kinases in Lipopolysaccharide Signaling

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