The measurement of pro-inflammatory cytokines IL-1��, IL-6, chemokine IL-8, and vascular endothelial growth factor signaling protein was carried out by quantifying mRNA expression levels as described previously. We investigated these factors due to their role in the host response during GBS infection of brain endothelium and other cell types. SVG-A cells were infected with GBS over time as described in Materials and Methods and transcript abundance ofIL-1��, IL-6, IL-8and VEGF were measured and normalized to the expression level of GAPDH housekeeping gene and compared to uninfected controls. All cytokines were significantly induced during GBS infection at all time points examined. An ELISA was performed to assay IL-8 protein levels, which demonstrated a significant increase in IL-8protein at 4hours post GBS infection. These results are the first to Quinapril hydrochloride demonstrate that GBS infection induces as Triamcinolone trocytecytokine production, which may contribute to the increase in meningeal inflammation. We hypothesize that once the GBS penetrates brain endothelial cells and gains access to astrocytes, GBS further induces an astrocytic inflammatory response, which could impact endothelial barrier integrity. IL-8isapotent neutrophil chemokine that is involved in neutrophil activation and recruitment neutrophil migration has been shown to promote BBB permeability during experimental GBS meningitis. Secretion of cytokines and chemokines by astrocytes may allow GBS to penetrate further through the BBB, thus, contributing to the progression of meningitis. Alternatively, this immune response may represent an effective second line of host defense or neuro protection, preventing further penetration of GBS into the CNS. However, subsequent increases in proinflammatory pathways produced after GBS infection, could intensify the permeability or leakiness of the BBB resulting in further exacerbation or the development of meningitis. Interestingly VEGF, which increases brain endothelial permeability when given intravenously, is neuroprotective and reduces BBB leakage after ischemia when given intraventricularly.