Petit J C
Infect Immun. 1980 Jan;27(1):61-7. doi: 10.1128/iai.27.1.61-67.1980.
Infection with Listeria monocytogenes was studied in strains of mice with genetic absence of the fifth component of complement (C5). Mice deficient in C5 consistently showed an increased growth of Listeria in their spleens as compared to normal mice. This increased growth was not corrected by administration of plasma containing C5. Furthermore, depletion of C5 and terminal complement components by administration of cobra venom factor did not impair the resistance to Listeria infection of normal mice. No phagocytic defect could be detected in macrophages from strains lacking C5. Transfer of bone marrow cells from C5+ but not from C5- mice corrected the marked increase of Listeria growth in mice having blockade of the reticuloendothelial system. We hypothesize that the defect of mice lacking C5 lies not in the absence of serum C5 but somewhere at the level of the macrophage.
在缺乏补体第五成分（C5）的基因工程小鼠品系中，对单核细胞增生李斯特菌感染进行了研究。与正常小鼠相比，C5缺陷小鼠脾脏中李斯特菌的生长持续增加。给予含有C5的血浆并不能纠正这种生长增加。此外，给予眼镜蛇毒因子消耗C5和补体末端成分，并不损害正常小鼠对李斯特菌感染的抵抗力。在缺乏C5的品系的巨噬细胞中未检测到吞噬缺陷。从C5 +小鼠而非C5 -小鼠转移骨髓细胞，纠正了网状内皮系统被阻断的小鼠中李斯特菌生长的显著增加。我们推测，缺乏C5的小鼠的缺陷不在于血清C5的缺失，而在于巨噬细胞水平的某个部位。
