Mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing

作者：Susana Merino, Silvia Camprubí, Sebastián Albertí, Vicente Javier Benedi, Juan M. Tomás · 发表于：Infection and Immunity · 年份：1992 · DOI：10.1128/iai.60.6.2529-2535.1992 · 被引用次数：228 · 研究领域：Antibiotic Resistance in Bacteria、Bacterial Infections and Vaccines、Escherichia coli research studies

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.