Antibody-independent activation of the classical pathway of human serum complement by lipid A is restricted to re-chemotype lipopolysaccharide and purified lipid A.
Antibody-independent activation of the classical pathway of human serum complement by lipid A is restricted to re-chemotype lipopolysaccharide and purified lipid A.
复制标题
脂质 A 对人血清补体经典途径的抗体依赖性激活仅限于重新化学型脂多糖和纯化的脂质 A。
DOI：
10.1128/iai.53.3.480-485.1986
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发表时间：
1986
影响因子：
3.1
通讯作者：
Vukajlovich,SW
中科院分区：
文献类型：
--
作者：
Vukajlovich,SW
大多数细菌脂多糖（LPS）与正常人血清在37 ℃下孵育可激活血清补体系统，导致溶血性补体水平降低。一组从沙门氏菌粗糙突变株分离的R-化学型LPS制剂，以及来自沙门氏菌的光滑野生型LPS。使用大肠杆菌O 55-B5、粘质沙雷氏菌和小肠炎耶尔森氏菌，检测LPS多糖链长度对LPS脂质（脂质A）依赖性补体经典途径（CPC）活化的影响。为了检测CPC的特异性脂质A依赖性活化，通过去除因子D制备补体活性旁路途径缺陷的血清。用福尔马林化兔红细胞吸收正常人血清被发现可以去除天然抗体、能够形成激活CPC的LPS复合物的因子或两者。通过使用这样的因子D耗尽的福尔马林化兔红细胞吸收的正常人血清，发现仅分离的脂质A和Re-chemotype LPS（R595 LPS）激活CPC。因此，与缺乏L-甘油-D-甘露庚糖的Re-化学型LPS结构相比，Rd 2 LPS寡糖链中存在额外的单糖L-甘油-D-甘露庚糖足以阻断LPS对CPC的脂质A依赖性活化。
Incubation of most bacterial lipopolysaccharides (LPS) with normal human sera at 37 degrees C activates the serum complement system, resulting in decreased levels of hemolytic complement. A panel of R-chemotype LPS preparations isolated from Salmonella minnesota rough mutant strains, as well as smooth wild-type LPS from S. minnesota, Escherichia coli O55-B5, Serratia marcescens, and Yersinia enterolitica, were used to examine the effect of LPS polysaccharide chain length on LPS lipid (lipid A)-dependent activation of the classical pathway of complement (CPC). To examine specific lipid A-dependent activation of the CPC, sera deficient in alternative pathway of complement activity were prepared by the removal of factor D. Absorption of normal human sera with formalinized rabbit erythrocytes was found to remove natural antibodies, factors capable of forming LPS complexes which activate the CPC, or both. By using such factor D-depleted formalinized rabbit erythrocyte-absorbed normal human sera, only isolated lipid A and Re-chemotype LPS (R595 LPS) were found to activate the CPC. Thus, the presence of the additional monosaccharide L-glycero-D-mannoheptose in the Rd2 LPS oligosaccharide chain compared with the L-glycero-D-mannoheptose-deficient Re-chemotype LPS structure is sufficient to block lipid A-dependent activation of the CPC by LPS.