Group B streptococci (GBS) are an important cause of neonatal sepsis, pneumonia and meningitis. In some newborns, GBS sepsis may have a severe course, including septic shock with high mortality rate, whereas other newborns are colonized with GBS on their surfaces without any clinical signs of bacterial infections. Interferon (IFN)-γ is produced in neonatal GBS sepsis, and transforming growth factor (TGF)-β is also found in the uterus. The involvement of IFN-γ and TGF-β in the earliest phase of infection might be a determinant of susceptibility and/or progression of infection in vivo. The aim of this study was to assess the effect of IFN-γ and TGF-β on adherence and intracellular viability in ECV304 cells of GBS serotype III isolated from cerebrospinal fluid (CSF) and vagina (strains 90356 and 80340, respectively). Interaction of GBS-ECV304 cells showed that the CSF isolate exhibited a more efficient adherence mechanism than the vagina isolate (P<0.001). Intracellular viability was observed for the CSF 90356 isolate within 2 h incubation. Results suggest the expression of additional bacterial virulence factors that favor some GBS type III strains to cause invasive disease. Detection of genotypic virulence marker (162-kb) in the CSF 90356 isolate by PFGE emphasizes the high risk of invasive infection by some GBS-III strains. Treatment of ECV304 cells with IFN-γ and/or TGF-β increased adherence of both GBS strains (P<0.001). Intracellular survival of the CSF 90356 isolate was observed after 24 h incubation following treatment of ECV304 cells with IFN-γ and TGF-β. Our data suggest that both IFN-γ and TGF-β may favor virulence of GBS strains. Variation of IFN-γ and TGF-β producing capacity of host cells of different individuals may influence development of invasive disease by GBS-III.

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