Interação de estreptococos do grupo B com células endoteliais humanas: papel do IFN-gama e expressão de ICAM-1

Abstract

Group B streptococcus (GBS) are the most common cause of pneumonia and sepsis during the neonatal period, which is mediated in part by cytokines. Neonatal sepsis has been associated with increased plasma concentrations of tumor necrosis factor-alfa (TNF), interferon-gamma (IFNg), ICAM-1 and ICAM-1 soluble form (sICAM-1). However, the mechanism by which GBS interacts with human cells and disrupts physiological processes is an intriguing area of investigation and continues to unfold. The aim of this study was to investigate the adherence and intracellular viability within human endothelial cells of GBS serotype III from neonate. GBS 90356-liquor exhibited a reduction on adherence (1h and 4h) and survival (4h) mechanisms to endothelial cells treated with IFN-gamma. In contrast, an efficient adherence and intracellular viability were verified in HUVEC treated with IFN plus TNF cytokines. Results of imunofluorescence and flow cytometry analysis showed that ICAM-1 molecules increased after HUVEC pre-treated with IFN, TNF, IFN plus TNF and infected with GBS. Moreover, sICAM-1 in supernatant was increased by the same treatments. SDS-PAGE analysis of samples of biotinylated HUVEC extracts treated with cytokines revealed fragments ranging from ~24 to ~146 kDa. Cytokines induced alterations on HUVEC surface molecules might be involved in the adherence, survival and an earlier onset of innate immune responses during GBS infections. These findings add to the current understanding of the roles played by multiple receptor-ligand systems in the uptake and pathogenesis of GBS infection. In conclusion, the molecular strategies displayed by GBS to interact with host cells in vitro are highly specific. Additional studies are necessary to identify which surface molecules present in GBS and HUVEC interplay the interaction between them.