Dankert J R
Department of Comparative and Experimental Pathology, University of Florida, Gainesville 32610.
Infect Immun. 1991 Jan;59(1):109-13. doi: 10.1128/iai.59.1.109-113.1991.
Investigation into the action of osmotically introduced C9 in Escherichia coli (in the absence of any other complement components) revealed that C9 could inhibit inner membrane respiration and cause a decrease in the viability of cells that were normally complement sensitive. This effect is analogous to the loss of inner membrane function and viability due to the assembly of the C5b-9 complex on these cells. Complement-resistant cells showed no such inhibition of respiration or loss of viability when subjected to the osmotic introduction of C9. The reason for this failure of C9 to affect complement-resistant cells was explored to determine whether this resistance to C9 was due to an inability of proteins in general to be osmotically introduced into the complement-resistant cells. The protein toxins melittin and colicin E1 were showed to be able to kill these complement-resistant cells (as well as complement-sensitive cells) when osmotically introduced into the periplasm. Therefore, cellular resistance to osmotically introduced C9 is not due to an inability of proteins to be introduced into the cells and may be related to a mechanism of cellular resistance to the C5b-9 complex.
对在大肠杆菌中通过渗透方式引入的C9（在不存在任何其他补体成分的情况下）的作用进行的研究表明，C9可抑制内膜呼吸，并导致通常对补体敏感的细胞活力下降。这种效应类似于由于C5b - 9复合物在这些细胞上组装而导致的内膜功能丧失和细胞活力下降。当对补体抗性细胞进行C9的渗透引入时，未观察到这种呼吸抑制或活力丧失。研究了C9无法影响补体抗性细胞的原因，以确定这种对C9的抗性是否是由于一般蛋白质无法通过渗透方式引入补体抗性细胞。当通过渗透方式引入周质时，蛋白质毒素蜂毒肽和大肠杆菌素E1能够杀死这些补体抗性细胞（以及补体敏感细胞）。因此，细胞对渗透引入的C9的抗性并非由于蛋白质无法引入细胞，可能与细胞对C5b - 9复合物的抗性机制有关。
