Mechanisms of Klebsiella pneumoniae resistance to complement-mediated killing.
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.
Merino
S
S
Departamento de Microbiología, Universidad de Barcelona, Spain.
Camprubí
S
S
Albertí
S
S
Benedí
V J
VJ
Tomás
J M
JM
D001770:Blood Bactericidal Activity; D003179:Complement C3b / Q000378:metabolism; D015938:Complement Membrane Attack Complex / Q000378:metabolism; D003165:Complement System Proteins / Q000502:physiology*; D006801:Humans; D007711:Klebsiella pneumoniae / Q000276:immunology*; D008070:Lipopolysaccharides / Q000378:metabolism
D015938:Complement Membrane Attack Complex; D008070:Lipopolysaccharides; D003179:Complement C3b; D003165:Complement System Proteins