Cavaillon J M, Fitting C, Caroff M, Haeffner-Cavaillon N
Unité d'Immuno-Allergie, Institut Pasteur, Paris, France.
Infect Immun. 1989 Mar;57(3):791-7. doi: 10.1128/iai.57.3.791-797.1989.
The capacities of lipopolysaccharide (LPS) and lipid A to trigger mouse BALB/c peritoneal macrophages and to induce the production of cell-associated interleukin-1 (IL-1) and membrane-associated IL-1 and IL-1 release have been compared. Bordetella pertussis lipid A was 1,000 to 10,000 times less efficient than the native LPS to induce IL-1 release by freshly isolated elicited macrophages. When resident macrophages were studied, lipid A, at high concentrations (greater than 2 micrograms/ml), induced significant levels of cell-associated IL-1 but little or no IL-1 release. With synthetic lipid A built up with the Escherichia coli lipid A structure (compound 506), IL-1 activity was present in the supernatants of elicited peritoneal macrophages and to a lesser extent in those of resident macrophages. However, the release of IL-1 induced by synthetic lipid A 506 remained much lower than those induced by rough LPS. Membrane-associated IL-1 could be induced on BALB/c macrophages with LPS and natural or synthetic lipid A, the LPS being the most active. In C3H/HeJ mice, neither natural nor synthetic lipid A could induce detectable cell-associated IL-1, whereas LPS could induce cell-associated and membrane IL-1 activity but no IL-1 release. Our results indicate that fragments of endotoxins may induce the production of IL-1 but the entire structure of the LPS molecule is the most effective to induce intracellular IL-1 production, expression of membrane IL-1, and release of IL-1.
已比较了脂多糖（LPS）和脂质A激发小鼠BALB/c腹膜巨噬细胞以及诱导细胞相关白细胞介素-1（IL-1）产生、膜相关IL-1和IL-1释放的能力。百日咳博德特氏菌脂质A诱导新鲜分离的致敏巨噬细胞释放IL-1的效率比天然LPS低1000至10000倍。当研究驻留巨噬细胞时，高浓度（大于2微克/毫升）的脂质A可诱导显著水平的细胞相关IL-1，但很少或不释放IL-1。对于由大肠杆菌脂质A结构构建的合成脂质A（化合物506），致敏腹膜巨噬细胞的上清液中存在IL-1活性，驻留巨噬细胞的上清液中IL-1活性较低。然而，合成脂质A 506诱导的IL-1释放仍远低于粗糙LPS诱导的释放。LPS以及天然或合成脂质A均可在BALB/c巨噬细胞上诱导膜相关IL-1，其中LPS活性最强。在C3H/HeJ小鼠中，天然或合成脂质A均不能诱导可检测到的细胞相关IL-1，而LPS可诱导细胞相关和膜IL-1活性，但不释放IL-1。我们的结果表明，内毒素片段可能诱导IL-1的产生，但LPS分子的完整结构对于诱导细胞内IL-1产生、膜IL-1表达和IL-1释放最为有效。
