Tanamoto K, Abe C, Homma J Y, Kojima Y
Eur J Biochem. 1979 Jul;97(2):623-9. doi: 10.1111/j.1432-1033.1979.tb13152.x.
Resistance against ascites tumor development and interferon-inducing activity were demonstrated in lipopolysaccharide derived from the protein-lipopolysaccharide complex obtained from an autolysate of Pseudomonas aeruginosa. Lipid A obtained from the lipopolysaccharide was sufficient to induce interferon in vitro but no antitumor activity was found if lipid A or the polysaccharide derived from lipopolysaccharide was injected into the animal. Chemical modification of the polysaccharide portion or deacylation of the lipopolysaccharide also diminished antitumor activity. In contrast, interferon was induced by these incomplete lipopolysaccharides. These results indicate that both the lipid A portion and covalently linked polysaccharide are necessary for the inhibition of ascites tumor development, whereas incomplete lipid A with amide-linked fatty acids is sufficient to induce interferon in vitro.
从铜绿假单胞菌自溶产物中获得的蛋白质 - 脂多糖复合物衍生的脂多糖表现出对腹水肿瘤发展的抗性和干扰素诱导活性。从脂多糖中获得的脂质A足以在体外诱导干扰素,但如果将脂质A或脂多糖衍生的多糖注射到动物体内,则未发现抗肿瘤活性。多糖部分的化学修饰或脂多糖的脱酰作用也会降低抗肿瘤活性。相反,这些不完全的脂多糖可诱导干扰素。这些结果表明,脂质A部分和共价连接的多糖对于抑制腹水肿瘤发展都是必需的,而具有酰胺连接脂肪酸的不完全脂质A足以在体外诱导干扰素。