Kochi S K, Johnson R C
Department of Microbiology, Medical School, University of Minnesota, Minneapolis 55455.
Infect Immun. 1988 Feb;56(2):314-21. doi: 10.1128/iai.56.2.314-321.1988.
The antibody and complement requirements for killing of Borrelia burgdorferi 297 by normal human serum (NHS) and NHS plus immunoglobulin G (IgG) were examined. B. burgdorferi activated both the alternative and classical complement pathways in NHS. In NHS chelated with 10 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid plus 4 mM MgCl2 (Mg-EGTA) to block classical pathway activation, consumption (activation) of total hemolytic complement, complement component 3 (C3), and C9 by B. burgdorferi was observed. Furthermore, challenge of unchelated NHS with 297 cells resulted in the consumption of C4, in addition to an increase in C3 and C9 consumption over that observed in chelated serum. In spite of complement activation, B. burgdorferi was resistant to the nonspecific bactericidal activity of NHS. The addition of human anti-B. burgdorferi IgG to NHS, however, resulted in the complete killing of 297 cells. Bactericidal activity of this serum was abrogated if NHS was immunochemically depleted of C1, indicating that killing was mediated by the classical pathway. The manifestation of bactericidal activity was accompanied by a large increase in total complement and C3 consumption over that observed in NHS alone. Under similar conditions, only a minimal increase in C9 consumption was observed. No increase in total complement consumption was observed if NHS plus anti-B. burgdorferi IgG was treated with Mg-EGTA prior to challenge. The results of these experiments demonstrate that B. burgdorferi is resistant to the nonspecific bactericidal activity of NHS, in spite of classical and alternative complement pathway activation. B. burgdorferi is sensitive to serum, however, in the presence of IgG, which mediates bacterial killing through the classical complement pathway.
研究了正常人血清（NHS）以及NHS加免疫球蛋白G（IgG）对杀灭伯氏疏螺旋体297的抗体和补体需求。伯氏疏螺旋体在NHS中激活了替代补体途径和经典补体途径。在与10 mM乙二醇双（β-氨基乙醚）-N，N，N'，N'-四乙酸加4 mM氯化镁（Mg-EGTA）螯合以阻断经典途径激活的NHS中，观察到伯氏疏螺旋体对总溶血补体、补体成分3（C3）和C9的消耗（激活）。此外，用297细胞攻击未螯合的NHS，除了C3和C9的消耗比在螯合血清中观察到的增加外，还导致C4的消耗。尽管补体被激活，但伯氏疏螺旋体对NHS的非特异性杀菌活性具有抗性。然而，向NHS中添加人抗伯氏疏螺旋体IgG导致297细胞被完全杀灭。如果NHS通过免疫化学方法去除C1，则该血清的杀菌活性被消除，表明杀灭是由经典途径介导的。杀菌活性的表现伴随着总补体和C3消耗比单独在NHS中观察到的大幅增加。在类似条件下，仅观察到C9消耗的最小增加。如果在攻击前用Mg-EGTA处理NHS加抗伯氏疏螺旋体IgG，则未观察到总补体消耗的增加。这些实验结果表明，尽管经典补体途径和替代补体途径被激活，但伯氏疏螺旋体对NHS的非特异性杀菌活性具有抗性。然而，在存在IgG的情况下，伯氏疏螺旋体对血清敏感，IgG通过经典补体途径介导细菌杀灭。
