810 Mechanism of Serum Resistance in Bacteria

Opt imum killing of gram-negative bacteria in serum requires the participation of terminal components of the complement system, presumably through formation of a membrane attack complex (MAC) 1 containing complement components C5b6789 (13). Although it is clear that some gram-negative bacteria are highly resistant to serum killing in the presence of adequate antibody, the mechanism of this resistance is not known. In the preceding paper (4), we reported results of uptake and consumption of C3 and terminal complement components by a smooth, serum-resistant strain of Salmonella minnesota ($218) and a rough, serum-sensitive mutant (Re595) of the above parent strain. We concluded that the mechanism of serum resistance in S. minnesota $218 does not involve a block in complement activation or in terminal complement component deposition on the bacterial surface but appears to be associated with a failure of the components to remain surface bound. In this paper, we report studies on the mechanism of terminal component consumption and release from S. minnesota $218. Our results show that binding of C8 and C9 to stably bound C5b67 on the bacterial surface of $218 results in release of the MAC without bacterial killing. The release of C5b-8 and C5b-9 appears to be associated with failure of the complexes to bind hydrophobically in the outer membrane.