Survival ofSerratia marcescensin the Presence of Complement

Abstract

Serratia marcescens has been isolated from a variety of ocular infections and:or in ammation. In order to survive in the eye, strains must be able to resist host defence systems. Complement has been shown to have an increased concentration and to be active during sleep. Not only is the complement system involved in host defence, but its activation can also produce in ammation. The aim of the present study was to examine the ability of ocular isolates of S. marcescens to withstand complement attack, activate complement and to examine the mechanisms used for evasion of this host defence system. The majority of isolates tested (4:6) were resistant to complement attack. These isolates were able to activate both complement pathways, as detected by enzyme-linked immunosorbent assays (ELISA) and western blotting assays. Components detected included C4, Factor B, C3 and C5. Possible mechanisms of resistance were elucidated including quantity of lipopolysaccharide (LPS) on the cell surface, ability to bind lactoferrin, types of complement components deposited onto the surfaces of strains, and the amount and location of C3 bound on the surface, as determined by transmission electron microscopy. Complement-resistant strains generated iC3b, bound more lactoferrin (1.7 9 0.6 for resistant cells compared with 0.4 90.2 for complement-sensitive cells, relative values), and had larger amounts of extractable endotoxin (216.8 988.8 m g:ml for resistant strains and 36.0 948.4 mg:ml for sensitive strains). Although there was no direct correlation between the ability to resist and activate complement and the isolation of strains from symptomatic or asymptomatic eyes, the resistance of strains to complement may allow these strains to remain in the eye and the activation of complement may contribute to the in ammatory response seen during infection or ocular in ammation.

Evasion of Cellular Ocular Defenses by Contact Lens Isolates of Serratia marcescens

“…When the strains were opsonized, both SVH and Smar 2 were sensitive to phagocytosis by PMNs. These two strains also were sensitive to complement attack, 12 which suggests a common mechanism for the serum-resistant strains in both assays. The activation of the respiratory burst and the resistance to phagocytic killing by PMNs may contribute to corneal destruction and inflammation in MK or further inflammation in adverse responses such as CLARE.…”

Induction of cytokines from polymorphonuclear leukocytes and epithelial cells by ocular isolates ofSerratia marcescens

“…It has been shown that S. marcescens can grow in the presence of lysozyme and lactoferrin 8 as well as complement. 9 However, it is unknown how these bacteria are able to initiate infection or inflammation. Bacteria are known to induce cytokines that may enhance polymorphonuclear leukocyte (PMN) infiltration into the cornea.…”