| Literature DB >> 1587619 |
S Merino1, S Camprubí, S Albertí, V J Benedí, J M Tomás.
Abstract
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.Entities:
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Year: 1992 PMID: 1587619 PMCID: PMC257192 DOI: 10.1128/iai.60.6.2529-2535.1992
Source DB: PubMed Journal: Infect Immun ISSN: 0019-9567 Impact factor: 3.441