Figure 8.
IL-1β is responsible for gp120-mediated upregulation of neuronal FHC. A, Neuronal/glial cocultures were treated with gp120IIIB (200 pm, 24 h) in the presence or absence of a TNF-α neutralizing antibody (40 μg/ml, 24 h). The neutralizing TNF-α antibody is unable to prevent gp120-induced increases in neuronal FHC (n = 3; compared with vehicle). B, C, Cocultures were treated with gp120IIIB (200 pm, 24 h) in the presence or absence of either a neutralizing IL-1β antibody (50 μg/ml, 24 h) or the IL-1 receptor antagonist (1 μg/ml, 24 h). Neutralization of IL-1β or antagonism of IL-1R1β reduces significantly the ability of gp120IIIB to upregulate protein levels of neuronal FHC (n = 3; compared with vehicle). D, Neurons cultured in the presence of a glial feeder layer (8 DIV) were treated with gp120BaL (200 pm, 24 h) in the presence or absence of the IL-1β neutralizing antibody (50 μg/ml, 24 h) or IL-1Ra (1 μg/ml, 24 h). Similar to the effects observed with gp120IIIB, antagonism or neutralization of IL-1β prevents neuronal FHC upregulation induced by gp120BaL (n = 3; compared with vehicle). ***p < 0.001.