Group B Streptococcus (GBS) is a major cause of maternal, fetal and neonatal morbidity and mortality worldwide. The transition from asymptomatic colonizer to invasive pathogen is not yet known, but it certainly correlates with a number of virulence factors. One of the most important is the capsule by which GBS binds regulatory components of the complement and thereby avoids recognition by the host immune system. In addition, the surface protein β has been shown to prevent opsonization by C3b by binding factor H (FH). In our experiment, we verified the latter by labeling with anti-C3b/iC3b and anti-FH antibodies and observed their binding to the capsule of bacteria previously exposed to the human serum. We also observed the survival of the bacteria in serum. The aim of the studywas to determine whether and how GBS strains, belonging to different serotypes and containing different virulence factors, bind and activate the complement system. In the study, virulently different GBS strains and control E. coli strains with different types of LPS were used. Binding of C3b/iC3b and FH was interpreted along with viability results. Differences in C3b/iC3b and FH binding were found between different GBS serotypes as well as between strains of the same capsular serotype. However, we found that the amount of FH and C3b/iC3b bound did not always increased survival. We also did not find a strong correlation between the expression of β protein and increased viability.
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