Abstract
Endothelial dysfunction is a major component of the pathophysiology of septicaemic group B Streptococcus (GBS) infections. Although cytokines have been shown to activate human umbilical vein endothelial cells (HUVECs), the capacity of interferon (IFN)-γ to enhance the microbicidal activity of HUVECs against GBS has not been studied. We report that the viability of intracellular bacteria was reduced in HUVECs activated by IFN-γ. Enhanced fusion of lysosomes with bacteria-containing vacuoles was observed by acid phosphatase and the colocalisation of Rab-5, Rab-7 and lysosomal-associated membrane protein-1 with GBS in IFN-γ-activated HUVECs. IFN-γ resulted in an enhancement of the phagosome maturation process in HUVECs, improving the capacity to control the intracellular survival of GBS.
Highlights
Group B Streptococcus (GBS) bacteria are a leading cause of life-threatening infections in neonates and young infants (Baker 2013)
We investigated whether IFN-γ contributes to bacteria killing via human umbilical vein endothelial cells (HUVECs)
We have shown in a previous study that human endothelial cells internalise group B Streptococcus (GBS), but do not efficiently eliminate internalised bacteria (Lione et al 2010), which most likely and partially stems from the low indices of endosomelysosome fusion observed in GBS-infected HUVECs
Summary
Group B Streptococcus (GBS) bacteria are a leading cause of life-threatening infections in neonates and young infants (Baker 2013). We investigated whether IFN-γ contributes to bacteria killing via human umbilical vein endothelial cells (HUVECs).
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