This product is extracted from E. coli serotype O111:B4 and purified by gel filtration. The source strain is from a private collection. This LPS serotype has been used to stimulate B-cells and induce NOS in human hepatocytes.
Lipopolysaccharides (LPSs) are characteristic components of the cell wall of Gram-negative bacteria. LPS and its lipid A moiety stimulate cells of the innate immune system by the Toll-like receptor 4 (TLR4), a member of the Toll-like receptor protein family, which recognizes common pathogen-associated molecular-patterns (PAMPs).
Lipopolysaccharide (LPS) is vital to both the structural and functional integrity of the Gram-negative bacterial outer membrane. Ubiquitously expressed by all Gram-negative bacteria, and containing several well-conserved domains, lipopolysaccharide also serves as one of the primary targets of the innate arm of the mammalian immune system. The lipopolysaccharides have a profound effect on the mammalian immune system and are of great significance in the pathophysiology of many disease processes.[1]
In vitro study indicated that the bone resorption and the inhibition of collagen synthesis caused by lipopolysaccharide could be prevented by PB effectively. Lipopolysaccharide at a concentration of 10μg /ml inhibited bone collagen synthesis by 43% and PB reversed this inhibition in a dose-dependent manner. Even at concentrations as low as 5 μg/ml (PB: LPS =1:2) it reduced the bone-resorbing activity of the lipopolysaccharide by 85%. This effect was specific for resorption stimulated by lipopolysaccharide.[2]
Lipopolysaccharide preconditioning to mice obviously reduced coelenterazine-Induced fluorescent lesions of Colon26 cells at 7 and 14 days after the intraportal inoculation of Colon26 cells, which expressed Nano-lantern, in comparison to control mice. Moreover, lipopolysaccharide preconditioning significantly reduced the fluorescence intensity of tumors than that of the control mice at both 7 and 14 days after tumor inoculation as well as reduced the liver weight in comparison to control mice at 14 days. Results showed that tumor metastasis was exclusively found in the lungs but not liver. Lipopolysaccharide preconditioning also tended to reduce lung metastasis in vivo.[3]
References:
[1]. Erridge C, et al. Structure and function of lipopolysaccharides. Microbes Infect. 2002 Jul;4(8):837-51.
[2]. Harvey W, et al. In vitro inhibition of lipopolysaccharide-induced bone resorption by polymyxin B. Br J Exp Pathol. 1986 Oct;67(5):699-705.
[3]. Nishikawa M, et al. Lipopolysaccharide preconditioning reduces liver metastasis of Colon26 cells by enhancing antitumor activity of natural killer cells and natural killer T cells in murine liver. J Gastroenterol Hepatol. 2021 Jul;36(7):1889-1898.
这个产品是从大肠杆菌O111:B4中提取的,并通过凝胶过滤纯化。源菌株来自私人收藏。这种LPS血清型已被用于刺激B细胞并在人类肝细胞中诱导NOS。
脂多糖（LPS）是革兰氏阴性菌细胞壁的特征成分。LPS及其脂质A部分通过Toll样受体4（TLR4）刺激先天免疫系统中的细胞,TLR4是Toll样受体蛋白家族的一员,可以识别常见的病原相关分子模式（PAMPs）。
脂多糖（LPS）对于革兰氏阴性细菌的外膜结构和功能完整性至关重要。所有革兰氏阴性细菌都广泛表达LPS,并包含几个保守区域,因此LPS也是哺乳动物先天免疫系统主要攻击目标之一。 LPS对哺乳动物免疫系统有深远影响,在许多疾病过程中具有重要意义。[1]
实验室研究表明,PB可以有效地预防脂多糖引起的骨吸收和胶原合成抑制。浓度为10μg/ml的脂多糖可将骨胶原合成抑制43％,而PB则以剂量依赖方式逆转了这种抑制作用。即使在低至5 μg/ml（PB：LPS = 1:2）的浓度下,它也能将脂多糖引起的骨吸收活性降低85％。这种效应是特异性针对由脂多糖刺激引起的吸收现象。
给小鼠进行脂多糖预处理后,与对照组相比,在肝门注射Nano-lantern标记的Colon26细胞后7天和14天时,明显减少了Coelenterazine诱导的荧光损伤。此外,脂多糖预处理还显著降低了肿瘤在7天和14天时的荧光强度,并且在第14天减轻了肝重量。结果显示,只有肺部出现了转移性肿瘤而没有发现在肝内。同时,在体内也倾向于减少肺部转移。