Human periodontal ligament stromal cells (hPDLSCs) and gingival mesenchymal stromal cells (hGMSCs) are resident mesenchymal stromal cells (MSCs) of the periodontal tissue. The lipopolysaccharide (LPS) from Porphyromonas gingivalis is structurally distinct from that of other Gram-negative bacteria, and earlier studies linked this structural difference to a distinct virulence activity and the ability to activate toll-like receptor 2 (TLR-2), besides TLR-4 as commonly occurring upon LPS challenge. Later studies, in contrast, argue that TLR-2 activation by P. gingivalis LPS is due to lipoprotein contamination. In the present study, we aimed to define the influence of structure versus purity of P. gingivalis LPS on the immune response of hPDLSCs and hGMSCs. Cells were stimulated with commercially available “standard” P. gingivalis LPS, “ultrapure” P. gingivalis LPS, or “ultrapure” Escherichia coli LPS, and the expression of interleukin- (IL-) 8, IL-6, monocyte chemoattractant protein- (MCP-) 1, TLR-2, and TLR-4 was evaluated. The contribution of TLR-4 to the LPS-induced response was assessed using the specific TLR-4 inhibitor TAK-242. “Standard” P. gingivalis LPS induced significantly higher IL-8, IL-6, and MCP-1 production compared to the “ultrapure” LPS preparations, with no significant difference detectable for “ultrapure” LPS from P. gingivalis and E. coli. By using TAK-242, the response of hPDLSCs and hGMSCs to “ultrapure” LPS preparations was effectively inhibited to the levels comparable to those of nonstimulated controls. In contrast, high levels of response to “standard” LPS were observed, even in the presence of TAK-242. Our data show that the response of MSCs from periodontal tissue to LPS depends more on the purity of the LPS preparation than on the LPS source. Even a small amount of contaminating lipoproteins can drastically enhance the hPDLSCs’ and hGMSCs; responsiveness to P. gingivalis LPS, which might also contribute to the progression of periodontal disease.

中文翻译：

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人类牙周间质基质细胞从牙周组织对LPS的反应取决于纯度，而不取决于LPS来源。

人牙周膜间质细胞（hPDLSC）和牙龈间质间质细胞（hGMSC）是牙周组织的常驻间质间质细胞（MSC）。牙龈卟啉单胞菌的脂多糖（LPS）在结构上不同于其他革兰氏阴性细菌，早期的研究将此结构差异与独特的毒力活性和激活Toll样受体2（TLR-2）的能力联系在一起。 LPS挑战时通常发生-4。相反，后来的研究认为，牙龈卟啉单胞菌LPS激活TLR-2是由于脂蛋白污染所致。在本研究中，我们旨在定义结构对齿龈假单胞菌纯度的影响。LPS对hPDLSC和hGMSC的免疫反应。用市售的“标准”牙龈卟啉单胞菌LPS，“超轻型”牙龈丙酸杆菌LPS或“超轻型”大肠杆菌LPS刺激细胞，并表达白介素-（IL-）8，IL-6，单核细胞趋化蛋白- （MCP-）1，TLR-2和TLR-4被评估。使用特定的TLR-4抑制剂TAK-242评估了TLR-4对LPS诱导的反应的贡献。与“超纯” LPS制剂相比，“标准”齿龈假单胞菌LPS诱导产生更高的IL-8，IL-6和MCP-1产量，而从齿龈假单胞菌和大肠杆菌中检测到的“超纯” LPS没有明显差异。。通过使用TAK-242，hPDLSC和hGMSC对“超纯” LPS制剂的反应被有效抑制到了与非刺激对照组相当的水平。相反，即使存在TAK-242，也观察到了对“标准” LPS的高水平反应。我们的数据表明，来自牙周组织的MSC对LPS的反应更多地取决于LPS制剂的纯度，而不是LPS来源。即使少量的污染性脂蛋白也可以大大增强hPDLSC和hGMSC。对牙龈卟啉单胞菌LPS的反应性，这也可能有助于牙周疾病的进展。