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Chapter 12 : Mechanism of Serum Resistance in Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures

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Mechanism of Serum Resistance in Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures, Page 1 of 2

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Abstract:

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. 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 . In both strains, RC1 and 811, the most abundant portion of C3b is inactivated and iC3b is the predominant molecule deposited on the surface.

Citation: Gundling F, Frosch M, Lüneberg E. 2002. Mechanism of Serum Resistance in Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures, p 60-63. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch12

Key Concept Ranking

Bacterial Proteins
0.67605776
Outer Membrane Proteins
0.55357146
Legionella pneumophila
0.4799739
0.67605776
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Figures

Image of FIGURE 1
FIGURE 1

C3 deposition on the cell surface of wild-type strain RC1 (A) and mutant 811 (B) from 40% normal human serum. The predominant 45-kDa band represents the iC3b molecule as immunostained with MAb 755. Reaction mixtures with serum replaced by buffer and with EGTA added to inhibit complement activation were included as controls. Application of identical amounts of protein to each lane was confirmed by silver-stained SDS gels run in parallel.

Citation: Gundling F, Frosch M, Lüneberg E. 2002. Mechanism of Serum Resistance in Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures, p 60-63. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch12
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Image of FIGURE 2
FIGURE 2

Quantification of C3a release (A) and C5a release (B) from 40% normal human serum after incubation with strains wild-type RC1 and mutant 811. For determination of C3a and C5a amounts, the ABICAP Immunoassay (Abion, Jülich, Germany) was used.

Citation: Gundling F, Frosch M, Lüneberg E. 2002. Mechanism of Serum Resistance in Comparison of Wild-Type and Mutant Strains after Phase Variation of Bacterial Surface Structures, p 60-63. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch12
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References

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