Analysis of complement C3 deposition and degradation on Klebsiella pneumoniae
Analysis of complement C3 deposition and degradation on Klebsiella pneumoniae
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DOI：
10.1128/iai.64.11.4726-4732.1996
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发表时间：
1996-11
影响因子：
3.1
通讯作者：
Sebastián Albertí;D. Álvarez;S. Merino;María Teresa Casado;Fernando Vivanco;Juan M. Tomás;V. Bened
中科院分区：
文献类型：
--
作者：
Sebastián Albertí;D. Álvarez;S. Merino;María Teresa Casado;Fernando Vivanco;Juan M. Tomás;V. Bened
大多数肺炎克雷伯氏菌血清耐药菌株激活补体并结合C3的调理素片段C3 b，而不形成C5 b-9和杀死细菌。研究了导致C3 b沉积而不发生细胞死亡的机制，结果表明，血清耐药菌株主要激活替代途径，而血清敏感菌株则激活替代途径和经典途径。与C3 b沉积有关的细菌分子是外膜孔蛋白和光滑和粗糙的脂多糖。孔蛋白激活两种补体途径，粗糙脂多糖激活经典途径，导致血清敏感菌株中C3 b沉积。抗血清菌株的光滑脂多糖仅激活旁路途径，阻碍C1 q与孔蛋白的结合（S。阿尔伯蒂湾马尔克斯岛坎普鲁比湾美利奴羊托马斯湾Vivanco，and V. J. Benedí，Infect. Immun. 61：852-860，1993; S. Alberti，F. Rodríguez-Quinónes，T. Schirmer，G. Rummel，J. M. Tomás，J. P. Rosenbusch，and V. J. Benedí，Infect. Immun. 63：903-910，1995）和粗糙脂多糖分子，从而防止经典途径的活化。在其沉积后，C3 b在两种类型的菌株上迅速降解为iC 3b，但由于替代和经典补体途径的激活，C3 b在血清敏感菌株上的较高水平沉积支持进一步的补体激活和血清敏感菌株的杀伤。
The majority of Klebsiella pneumoniae serum-resistant strains activate complement and bind C3b, the opsonic fragment of C3, without C5b-9 formation and bacterial killing. The mechanisms leading to C3b deposition without cell death were studied, and the results indicate that serum-resistant strains activate principally the alternative pathway and that serum-sensitive strains activate both the alternative and classical pathways. Bacterial molecules implicated in C3b deposition are the outer membrane porin proteins and smooth and rough lipopolysaccharides. Porins activate both complement pathways, and the rough lipopolysaccharide activates the classical pathway, causing deposition of C3b in serum-sensitive strains. The smooth lipopolysaccharide of serum-resistant strains activates only the alternative pathway, impeding the binding of C1q to porins (S. Albertí, G. Marqués, S. Camprubí, S. Merino, J. M. Tomás, F. Vivanco, and V. J. Benedí, Infect. Immun. 61:852-860, 1993; S. Albertí, F. Rodríguez-Quinónes, T. Schirmer, G. Rummel, J. M. Tomás, J. P. Rosenbusch, and V. J. Benedí, Infect. Immun. 63:903-910, 1995) and rough lipopolysaccharide molecules and thereby preventing activation of the classical pathway. After its deposition, C3b is quickly degraded to iC3b on both types of strains, but the higher-level deposition of C3b on serum-sensitive strains, resulting from activation of both the alternative and classical complement pathways, supports further complement activation and killing of serum-sensitive strains.