Nanoparticles (NPs) are easily contaminated by bacterial endotoxin (lipopolysaccharide [LPS]). The presence of LPS can be responsible for many immune/inflammatory effects attributed to NPs. In this study, we examined the effects of LPS adsorption on the NP surface on the formation of a biocorona in biological fluids and on the subsequent inflammation-inducing activity of NPs. Different gold (Au) NPs with sizes ranging from 10 to 80 nm and with different surface functionalization (sodium citrate, lipoic acid, and branched polyethyleneimine (BPEI), or polyethylene glycol (PEG)) were exposed to E. coli LPS under different conditions. The binding capacity of LPS to the surface of AuNPs was dose- and time-dependent. LPS attached to sodium citrate and lipoic acid coatings, but did not adhere to BPEI- or PEG-coated NPs. By computational simulation, the binding of LPS to AuNPs seems to follow the Langmuir absorption isotherm. The presence of LPS on AuNP surface interfered and caused a decrease in the formation of the expected biomolecular corona upon incubation in human plasma. LPS-coated AuNPs, but not the LPS-free NPs, induced significant inflammatory responses in vitro. Notably, while free LPS did also induce an anti-inflammatory response, LPS bound to NPs appeared unable to do so. In conclusion, the unintentional adsorption of LPS onto the NP surface can affect the biocorona formation and the inflammatory properties of NPs. Thus, for an accurate interpretation of NP interactions with cells, it is extremely important to be able to distinguish the intrinsic NP biological effects from those caused by biologically active contaminants such as endotoxin.

中文翻译：

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细菌内毒素（脂多糖）结合到金纳米颗粒的表面，干扰生物电晕的形成并诱导人类单核细胞的炎症激活

纳米颗粒（NPs）容易被细菌内毒素（脂多糖[LPS]）污染。LPS的存在可归因于NPs引起的许多免疫/炎症作用。在这项研究中，我们检查了LPS吸附在NP表面上对生物体液中生物电晕的形成以及对随后的NPs炎症诱导活性的影响。将大小在10至80 nm之间且具有不同表面功能化的不同金（Au）NP（柠檬酸钠，硫辛酸和支链聚乙烯亚胺（BPEI）或聚乙二醇（PEG））暴露于大肠杆菌LPS在不同条件下。LPS与AuNPs表面的结合能力是剂量和时间依赖性的。LPS附着在柠檬酸钠和硫辛酸涂层上，但不附着在BPEI或PEG涂层的NP上。通过计算模拟，LPS与AuNPs的结合似乎遵循Langmuir吸收等温线。在人血浆中孵育后，AuNP表面LPS的存在会干扰并导致预期的生物分子电晕的形成减少。涂有LPS的AuNPs，而不是不含LPS的NPs，在体外诱导出明显的炎症反应。值得注意的是，虽然游离的LPS确实也能诱导抗炎反应，但与NPs结合的LPS似乎不能这样做。总之，LPS意外吸附到NP表面会影响生物电晕的形成和NPs的炎症特性。因此，为了准确解释NP与细胞的相互作用，将内在的NP生物学效应与生物活性污染物（例如内毒素）引起的NP效应区分开是非常重要的。