Merino S, Camprubí S, Albertí S, Benedí V J, Tomás J M
Departamento de Microbiología, Universidad de Barcelona, Spain.
Infect Immun. 1992 Jun;60(6):2529-35. doi: 10.1128/iai.60.6.2529-2535.1992.
The different mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing were investigated by using different strains and isogenic mutants previously characterized for their surface components. We found that strains from serotypes whose K antigen masks the lipopolysaccharide (LPS) molecules (such as serotypes K1, K10, and K16) fail to activate complement, while strains with smooth LPS exposed at the cell surface (with or without K antigen) activate complement but are resistant to complement-mediated killing. The reasons for this resistance are that C3b binds far from the cell membrane and that the lytic final complex C5b-9 (membrane attack complex) is not formed. Isogenic rough mutants (K+ or K-) are serum sensitive because they bind C3b close to the cell membrane and the lytic complex (C5b-9) is formed.
通过使用先前已对其表面成分进行表征的不同菌株和同基因突变体，研究了肺炎克雷伯菌对补体介导杀伤的不同抗性机制。我们发现，来自K抗原掩盖脂多糖（LPS）分子的血清型的菌株（如血清型K1、K10和K16）无法激活补体，而细胞表面暴露有光滑LPS的菌株（无论有无K抗原）可激活补体，但对补体介导的杀伤具有抗性。这种抗性的原因是C3b在远离细胞膜的位置结合，且不会形成溶解性终末复合物C5b-9（膜攻击复合物）。同基因粗糙突变体（K+或K-）对血清敏感，因为它们在靠近细胞膜的位置结合C3b并形成溶解复合物（C5b-9）。
