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首页> 外文期刊>Cytokine >Porphyromonas gingivalis culture supernatants differentially regulate Interleukin-1beta and Interleukin-18 in human monocytic cells.
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Porphyromonas gingivalis culture supernatants differentially regulate Interleukin-1beta and Interleukin-18 in human monocytic cells.

机译：牙龈卟啉单胞菌培养物上清液差异调节人单核细胞中的白细胞介素-1β和白细胞介素18。

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Porphyromonas gingivalis is a major bacterial species implicated in chornic periodontitis, a disease characterized by inflammatory destruction of the tooth supporting tissues. Its main virulence factors are lipopolysaccharide (LPS) and gingipains, a group of cysteine proteinases. Interleukin (IL)-18 is a potent pro-inflammatory cytokine with structural similarities to IL-1beta. This study aimed to investigate if P .gingivalis regulates IL-1beta and IL-18 in monocytic cells. Monomac-6 cells were challenged with P. gingivalis culture supernatants. Quantitative real-time PCR and ELISA were used to investigate IL-1beta and IL-18 mRNA expression and protein secretion, respectively. P. gingivalis enhanced IL-1beta and IL-18 mRNA expression, the former being induced earlier, but transiently. IL-18 up-regulation was not affected by P. gingivalis heat-inactivation or chemical inhibition of its gingipains, whereas both treatments resulted in 50% reduction of IL-1beta expression. Purified P. gingivalis LPS enhanced both IL-1beta and IL-18 expression. However, only IL-1beta, but not IL-18, secretion was detected, and was up-regulated by P. gingivalis. In conclusion, although IL-1beta and IL-18 belong to the same cytokine family, their gene expression and secretion are differentially regulated in human monocytic cells in response to P. gingivalis. Therefore, cytokines of the IL-1 family may participate via different pathways in the complex pathogenesis of periodontitis.
机译：牙龈卟啉单胞菌（Porphyromonas gingivalis）是与角膜牙周炎有关的一种主要细菌，这种疾病的特征是牙齿支持组织的炎性破坏。它的主要毒力因子是脂多糖（LPS）和半胱氨酸蛋白酶，这是一组半胱氨酸蛋白酶。白介素（IL）-18是一种有效的促炎细胞因子，与IL-1beta具有结构相似性。这项研究旨在调查牙龈卟啉单胞菌是否调节单核细胞中的IL-1beta和IL-18。 Monomac-6细胞用牙龈卟啉单胞菌培养物上清液攻击。实时定量PCR和ELISA分别用于研究IL-1beta和IL-18 mRNA的表达以及蛋白质的分泌。牙龈卟啉单胞菌增强了IL-1β和IL-18 mRNA的表达，前者被诱导得较早，但是短暂的。 IL-18的上调不受牙龈卟啉单胞菌的热灭活或对其牙龈蛋白酶的化学抑制的影响，而两种处理均导致IL-1beta表达降低50％。纯化的牙龈卟啉单胞菌LPS增强IL-1beta和IL-18表达。但是，仅检测到IL-1β分泌，未检测到IL-18分泌，并且被牙龈卟啉单胞菌上调。总之，尽管IL-1β和IL-18属于同一细胞因子家族，但它们的基因表达和分泌在人单核细胞中对牙龈卟啉单胞菌的反应受到不同的调节。因此，IL-1家族的细胞因子可能通过不同的途径参与牙周炎的复杂发病机理。

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