Complement activation and C3 binding by serum-sensitive and serum-resistant strains of Pseudomonas aeruginosa

The relationship among complement consumption, C3 deposition, and C3 fragmentation pattern was compared for serum-sensitive (Ser(s)) and serum-resistant (Ser(r)) strains of Pseudomonas aeruginosa. The Ser(s) strains, which were mucoid strains derived from patients with cystic fibrosis, had lipopolysaccharide deficient in 0-antigen side chains. These organisms generally activated much less complement per organism than their Ser(r) counterparts, characterized by the presence of lipopolysaccharide with long lipopolysccharide 0 side chains. Surprisingly, however, although the Ser(r) strains consumed more total hemolytic complement, less C3 was deposited onto the surface of these strains than onto that of the Ser(s) strains. Maximal C3 binding required the participation of both the classical and alternative complement pathways, although classical complement pathway involvement was more important for Ser(r) strains. Finally, while more than half of the C3 deposited on most Ser(s) strains was in the form of C3b, most of the C3 on the Ser(r) strains was in the form of iC3b, indicating a more rapid and extensive conversion of C3b to iC3b on the surface of these strains. Limited complement activation by Ser(s) mucoid strains of P. aeruginosa may confer a selective survival advantage to these organisms in colonizing the airways of patients with cystic fibrosis.