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首页> 外文期刊>Infection and immunity >Insertional Inactivation of pac and rmlB Genes Reduces the Release of Tumor Necrosis Factor Alpha, Interleukin-6, and Interleukin-8 Induced by Streptococcus mutans in Monocytic, Dental Pulp, and Periodontal Ligament Cells
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Insertional Inactivation of pac and rmlB Genes Reduces the Release of Tumor Necrosis Factor Alpha, Interleukin-6, and Interleukin-8 Induced by Streptococcus mutans in Monocytic, Dental Pulp, and Periodontal Ligament Cells

机译：pac和rmlB基因的插入失活减少了变形链球菌在单核细胞，牙髓和牙周膜细胞中诱导的肿瘤坏死因子α，白细胞介素6和白细胞介素8的释放。

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Streptococcus mutans possesses different cell wall molecules, such as protein of the I/II family, the serotype f polysaccharide rhamnose glucose polymer (RGP), and lipoteichoic acid (LTA), which act as adhesins and modulins, allowing S. mutans to colonize teeth and cause dental caries and pulpitis. We tested several isogenic mutants of S. mutans defective in protein I/II and/or RGP, as well as purified modulins such as protein I/II, RGP, and LTA, for their binding and activation abilities on monocytic, dental pulp (DP), and periodontal ligament (PDL) cells. Our results demonstrate that both protein I/II and RGP play important roles in streptococcal adherence to human monocytic and fibroblastic cells, whereas LTA is only a minor adhesin. In the activation process, the cytokine response elicited is polarized toward a Th1 response which seems principally due to protein I/II and RGP. Even if protein I/II seems to be more efficient in its purified form in triggering cells to release interleukin-8 (IL-8), RGP is the most efficient cytokine-stimulating component in intact bacteria, while LTA plays only a minor role. In cell activation, we showed, by using either cytochalasin D or coated ligands, that internalization of either S. mutans, S. mutans isogenic mutants, or purified ligands is not necessary to trigger cells to release IL-8. We also showed that, besides the implication of monocytes in pulpal inflammation, fibroblast-like cells such as DP and PDL cells are also actively implicated in local inflammation and in the generation of a Th1 response after stimulation with S. mutans cells or antigens.
机译：变形链球菌具有不同的细胞壁分子，例如I / II家族的蛋白质，血清型f多糖鼠李糖葡萄糖聚合物（RGP）和脂磷壁酸（LTA），它们分别作为粘附素和调节素，允许 S。变种会使牙齿定居并引起龋齿和牙髓炎。我们测试了 S的几个同基因突变体。蛋白I / II和/或RGP以及纯化的调节蛋白（例如蛋白I / II，RGP和LTA）在单核细胞，牙髓（DP）和牙周膜上的结合和活化能力方面存在缺陷韧带（PDL）细胞。我们的结果表明，蛋白I / II和RGP在链球菌对人单核细胞和成纤维细胞的粘附中均起重要作用，而LTA只是次要的粘附素。在激活过程中，引起的细胞因子反应被极化为Th1反应，这主要归因于蛋白质I / II和RGP。即使蛋白质I / II以其纯化形式似乎在触发细胞释放白介素8（IL-8）方面更有效，RGP还是完整细菌中最有效的细胞因子刺激成分，而LTA仅起次要作用。在细胞活化中，我们通过使用细胞松弛素D或包被的配体显示了 S的内在化。变体， S。突变体同基因突变体或纯化的配体对于触发细胞释放IL-8并不是必需的。我们还表明，除了髓核炎症中涉及单核细胞外，成纤维样细胞（如DP和PDL细胞）还积极参与局部炎症和 S刺激后Th1反应的产生。变形细胞或抗原。

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