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首页> 美国卫生研究院文献>The Korean Journal of Physiology Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology >Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium
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Peptidoglycan Induces the Production of Interleukin-8 via Calcium Signaling in Human Gingival Epithelium

机译：肽聚糖通过人牙龈上皮中的钙信号传导诱导白介素8的产生。

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摘要

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of gram-positive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.
机译：牙周病的病因是多方面的。外源性刺激物（例如细菌病原体）可以与收费样受体相互作用，激活牙龈上皮和其他组织中的细胞内钙信号传导。钙信号的触发诱导促炎性细胞因子如白介素8的分泌，这是炎症反应的一部分。然而，当牙龈上皮细胞暴露于病原体时，细菌毒素诱导的钙信号传导的确切机制尚不清楚。在这里，我们调查细菌诱导的钙信号传导和人牙龈上皮细胞中炎性细胞因子的表达。我们发现，肽聚糖是革兰氏阳性细菌的组成部分，也是Toll样受体2的激动剂，以浓度依赖的方式增加细胞内钙。肽聚糖诱导的钙信号通过磷脂酶C（），肌醇1,4,5-三磷酸受体的阻滞剂治疗而被废除，表明钙从细胞内钙存储中释放。肽聚糖介导的白介素8表达被1,2-双（2-氨基苯氧基）乙烷-N，N，N'，N'-四乙酸四（乙酰氧基甲基酯）阻断。此外，当thapsigargin单独治疗或与肽聚糖共同治疗时，thapsigargin可以诱导白细胞介素8的表达，thapsigargin是肌氨酸/内质网钙ATP酶的选择性抑制剂。这些结果表明，革兰氏阳性细菌毒素肽聚糖通过磷脂酶C /肌醇1,4,5-三磷酸途径诱导钙信号传导，并且白细胞介素8表达的增加是由人牙龈上皮细胞中的细胞内钙水平介导的。

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