ANALYSIS OF COMPLEMENT C3 DEPOSITION AND DEGRADATION ON KLEBSIELLA-PNEUMONIAE

The majority of Klebsiella pneumoniae serum-resistant strains activate complement and bind C3b, the opsonic fragment of C3, without C5b-9 fo rmation and bacterial killing. The mechanisms leading to C3b depositio n without cell death were studied, and the results indicate that serum -resistant strains activate principally the alternative pathway and th at serum-sensitive strains activate both the alternative and classical pathways, Bacterial molecules implicated in C3b deposition are the ou ter membrane porin proteins and smooth and rough lipopolysaccharides, Porins activate both complement pathways, and the rough lipopolysaccha ride activates the classical pathway, causing deposition of C3b in ser um-sensitive strains, The smooth lipopolysaccharide of serum-resistant strains activates only the alternative pathway, impeding the binding of C1q to porins (S. Alberti, G. Marques, S. Camprubi, S. Merino, J. M . Tomas, F. Vivanco, and V. J. Benedi, Infect. Immun. 61:852-860, 1993 ; S. Alberti, F. Rodriguez-Quinones, T. Schirmer, G. Rummel, J. M. Tom as, J. P. Rosenbusch, and V. J. Benedi, Infect. Immun. 63:903-910, 199 5) and rough lipopolysaccharide molecules and thereby preventing activ ation of the classical pathway, After its deposition, C3b is quickly d egraded to iC3b on both types of strains, but the higher-level deposit ion of C3b on serum-sensitive strains, resulting from activation of bo th the alternative and classical complement pathways, supports further complement activation and killing of serum-sensitive strains.