High glucose-induced oxidative stress increases IL-8 production in human gingival epithelial cells

High glucose-induced oxidative stress increases IL-8 production in human gingival epithelial cells
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DOI:
10.1111/odi.12502
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发表时间:
2016-09-01
期刊:
影响因子:
3.8
通讯作者:
Murakami, S.
Murakami, S.
中科院分区:
医学3区
文献类型:
--
作者:
Kashiwagi, Y.;Takedachi, M.;Murakami, S.

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糖尿病通常与牙周病的患病率和严重程度增加有关。我们假设,牙龈上皮细胞修改牙周病的进展和预测,高血糖症将激活炎症反应在人牙龈上皮细胞(HGECs)。Materials and MethodsWe测试我们的假设在永生HGECs(表皮4细胞)从牙周组织分离和转染猿猴病毒40 T抗原。结果与正常对照组相比,高糖组epi 4细胞白细胞介素8(IL 8)蛋白分泌和mRNA表达均明显增加。这些效应与细胞增殖增加无关,并且在高渗对照组(正常葡萄糖和19 mM甘露醇)中未观察到。用抗氧化剂N-乙酰半胱氨酸或蛋白激酶C抑制剂Ro 31 -8220预处理可抑制HG中IL-8分泌增加。牙龈增生不影响牙龈成纤维细胞或牙周膜细胞分泌IL-8。在epi 4细胞中,高血糖也可诱导TLR 2的表达,但不诱导TLR 4的表达。
ObjectiveDiabetes is often associated with increased prevalence and severity of periodontal disease. We hypothesized that gingival epithelial cells modify periodontal disease progression and predicted that hyperglycemia would activate an inflammatory response in human gingival epithelial cells (HGECs).Materials and MethodsWe tested our hypothesis in immortalized HGECs (epi 4 cells) isolated from periodontal tissue and transfected with the simian virus 40 T antigen. The epi 4 cells were cultured in high (25mM, HG) and normal (6mM, NG) glucose conditions.ResultsThe epi 4 cells showed increased interleukin-8 (IL-8) protein secretion and mRNA expression when cultured in HG, compared with in NG. These effects were not associated with increased cell proliferation and were not observed in a hyperosmolar control group (normal glucose with 19mM mannitol). Increased IL-8 secretion in HG was inhibited by pretreatment with an antioxidant, N-acetylcysteine, or a protein kinase C inhibitor, Ro31-8220. Hyperglycemia did not affect IL-8 secretion by gingival fibroblasts or periodontal ligament cells. In epi 4 cells, hyperglycemia also induced expression of toll-like receptor 2 (TLR2) but not TLR4.ConclusionThese findings suggest a potential participation of epithelial cells in periodontal disease during diabetes by evoking an excessive host inflammatory response.