Many studies use human BMEC as an in vitro model to examine how GBS interactions enable endothelial penetration. Erythromycin However, while one study has demonstrated that GBS interacts directly with human fetal astrocytes, the nature of these interactions have not been thoroughly investigated. We hypothesize that astrocytes play a unique role in GBS infection and the development of meningitis. In the current study, we examined the capacity of GBS to attach, invade, survive intracellularly, and induce cytokine transcription in a human astrocyte cell line. We further identify GBS surface expressed factors that contribute to these interactions. Together these data confirm previous Puromycin dihydrochloride Reports and demonstrate that GBS has the capacity to adhere to and invade human astrocytes. Interestingly, after 4h of antibiotic treatment we observed an increase in the number of vesicles containing intracellular GBS present in SGV-A compared to the 2h time point. In addition, several bacteria appear to have septa that are indicative of bacterial division and vesicular-like structures appear to be fusing. Auto phagosomes are frequently observed fusing with endosomalor lysosomal vesicles and are double membrane structures. Reports show that in TEM plastic sections, the double membranes can be so close to each other that it is not possible to see them as separate membranes and sometimes the autophagosome limiting membrane does not have any contrast in thin sections. Although, the internal vesicles containing GBS may be reminiscent of auto phagosomes, we have not yet defined the nature of these compartments. These findings demonstrate that GBS isolates are able to adhere and invade astrocytes to varying degrees, which may be due to differences in cell surface expressed determinants resulting in divergent affinities or capacities for binding to human astrocytes. The variable invasiveness exhibited by the different GBS strains has been previously observed for other cell types such as human vaginal epithelial cells, human pulmonary alveolarepithelial cells, human umbilical vein endothelial cells, and human brain endothelial cells.