MESOPHILIC AEROMONAS SP SEROGROUP 0 11 RESISTANCE TO COMPLEMENT-MEDIATED KILLING/

The complement activation by and resistance to complement-mediated kil ling of Aeromonas sp. strains from serogroup O:11 were investigated by using different wild-type strains (with an S-layer characteristic of this serogroup) and their isogenic mutants characterized for their sur face components (S-layer and lipopolysaccharide [LPS]). All of the Aer omonas sp. serogroup O:11 wild-type strains are unable to activate com plement, which suggested that the S-layer completely covered the LPS m olecules. We found that the classical complement pathway is involved i n serum killing of susceptible Aeromonas sp. mutant strains of serogro up O11, while the alternative complement pathway: seems not to be invo lved, and that the complement activation seems to be independent of an tibody. The smooth mutant strains devoid of the S-layer (S-layer isoge nic mutants) or isogenic LPS mutant strains with a complete or rather complete LPS core (also without the S-layer) are able to activate comp lement but are resistant to complement-mediated killing. The reasons f or this resistance are that C3b is rapidly degraded, and therefore the lgtic membrane attack complex (C5b-9) is not formed. Isogenic LPS rou gh mutants with an incomplete LPS core are serum sensitive because the y bind more C3b than the resistant strains, the C3b is not completely degraded, and therefore the lytic complex (C5b-9) is formed.