Mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing.

S Merino; S Camprubí; S Albertí; V J Benedí; J M Tomás

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Mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing.

机译：肺炎克雷伯菌抵抗补体介导的杀伤的机制。

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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.

机译：肺炎克雷伯氏菌对补体介导的杀伤的抗药性的不同机制，是通过使用先前表征其表面成分的不同菌株和同基因突变体研究的。我们发现，其K抗原掩盖脂多糖（LPS）分子的血清型的菌株（例如血清型K1，K10和K16）无法激活补体，而在细胞表面暴露有光滑LPS的菌株（有或没有K抗原）都可以激活。补体，但对补体介导的杀伤具有抗性。产生这种抗性的原因是C3b与细胞膜的结合较远，并且未形成裂解性最终复合物C5b-9（膜攻击复合物）。等基因粗糙突变体（K +或K-）对血清敏感，因为它们结合靠近细胞膜的C3b并形成了裂解复合物（C5b-9）。

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《Infection and immunity》 |1992年第6期|共7页
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S Merino; S Camprubí; S Albertí; V J Benedí; J M Tomás;
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Mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing.

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