Summary
The mechanisms of bacterial resistance to complement-mediated killing were investigated. Initial studies showed that the C5b-9 complex of complement was formed rapidly on smooth, serum resistant (ser-R) Salmonella and E. coli strains incubated in serum. However, the complex did not insert into hydrophobic domains of the outer membrane, was shed from the bacterial surface and was not bactericidal. Recent work shows that complement is being deposited on only the longest lipopolysaccharide molecules in these strains, suggesting that C5b-9 is sterically blocked from access to complement susceptible sites on the outer membrane. Ser-R Neisseria gonorrhoeae (GC) also activate complement efficiently, but the non-bactericidal C5b-9 complex which forms on and remains stably bound to the outer membrane of ser-R GC is in a different molecular configuration than the bactericidal C5b-9 formed on serum-sensitive GC or ser-R GC rendered sensitive with antibody. Additional studies with polyclonal and monoclonal antibodies suggest that bactericidal antibody may function by increasing the bactericidal efficiency of C5b-9 in the bacterial surface.
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Joiner, K.A., Frank, M.M. (1985). Mechanisms of Bacterial Resistance to Complement-Mediated Killing. In: Jackson, G.G., Thomas, H. (eds) The Pathogenesis of Bacterial Infections. Bayer-Symposium, vol 8. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70351-5_11
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DOI: https://doi.org/10.1007/978-3-642-70351-5_11
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