Fig. 5

SP augments the production of inflammatory and neurotoxic mediators by bacterially challenged human astrocytes. Panel a U87-MG cells (labeled U87) or primary human astrocytes were untreated (0), or exposed to LPS (20–500 ng/mL) or bacterial flagellin plus Pam3Cys at 75 ng/mL and 500 ng/mL (lo) or 150 ng/mL and 1000 ng/mL (hi), respectively, in the absence (−SP) or presence (+SP) of recombinant SP (10 nM), for 24 h, and the level of IL-6 protein release was determined by specific capture ELISA (n = 3). Panel b Primary human astrocytes were untreated (0) or challenged with B. burgdorferi (MOI of 10 and 100:1 bacteria to human cells), N. meningiditis (Nm: MOI of 1 and 10:1), S. pneumoniae (Stp: MOI of 10 and 100:1), or S. aureus (Sa: MOI of 10 and 100:1), in the absence (−SP) or presence (+SP) of recombinant SP (5 nM), for 24 h and the level of IL-6 release was determined by specific capture ELISA (n = 3). Panel c Primary human astrocytes were untreated (0) or challenged with B. burgdorferi (MOI of 1, 10, and 100:1 bacteria to human cells) or S. pneumoniae (Stp: MOI of 1, 10, and 100:1), in the absence (−SP) or presence (+SP) of recombinant SP (5 nM) for 24 h. Conditioned medium from each was then placed on HCN neuronal cells and cell death was assessed by trypan blue exclusion at 24 h (n = 3). Data is expressed as the mean ± SEM and asterisks indicate statistically significant differences between the SP treated and untreated cells (p < 0.05)