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Chapter 12 : Mechanism of Serum Resistance in Legionella pneumophila: Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures
Mechanism of Serum Resistance in Legionella pneumophila: Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures, Page 1 of 2< Previous page Next page > /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap12-1.gif /docserver/preview/fulltext/10.1128/9781555817985/9781555812300_Chap12-2.gif
For pathogenic bacteria, evasion from lysis by serum complement factors in the human host is essential for survival and virulence. Therefore, many pathogens have developed effective strategies to overcome eradication by complement. Such strategies include removal or destruction of complement factors, inhibition of complement activation, or imitation of complement protein by molecular mimicry. Legionella pneumophila activates complement via both pathways, the classical and the alternative. Lipopolysaccharide (LPS) phase variation is associated with serum sensitivity and loss of virulence. Wild-type RC1 and the phase-variant mutant 811 exhibited significant differences with regard to resistance to serum complement factors. Strain RC1 was relatively serum resistant, whereas when mutant 811 was incubated with 40% normal human serum at 37№C, no viable bacteria were recovered after 15 min. Therefore, the two strains provide a valuable tool for comparative investigation of serum resistance in L. pneumophila. In both strains, RC1 and 811, the most abundant portion of C3b is inactivated and iC3b is the predominant molecule deposited on the L. pneumophila surface.