MECHANISMS OF KLEBSIELLA-PNEUMONIAE RESISTANCE TO COMPLEMENT-MEDIATED KILLING
MECHANISMS OF KLEBSIELLA-PNEUMONIAE RESISTANCE TO COMPLEMENT-MEDIATED KILLING
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DOI：
10.1128/iai.60.6.2529-2535.1992
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发表时间：
1992-06-01
影响因子：
3.1
通讯作者：
TOMAS, JM
中科院分区：
文献类型：
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作者：
MERINO, S;CAMPRUBI, S;TOMAS, JM
使用不同的菌株和同基因突变体，其特征在于其表面成分的肺炎克雷伯氏菌抵抗补体介导的杀伤的不同机制进行了研究。 我们发现，来自K抗原掩盖脂多糖（LPS）分子的血清型（如血清型K1，K10和K16）的菌株不能激活补体，而暴露在细胞表面的光滑LPS（有或没有K抗原）的菌株激活补体，但对补体介导的杀伤有抗性。 这种抗性的原因是C3 b结合远离细胞膜，并且没有形成裂解最终复合物C5 b-9（膜攻击复合物）。 同基因粗糙突变体（K+或K-）是血清敏感的，因为它们结合C3 b接近细胞膜和裂解复合物（C5 b-9）的形成。
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.