PKC activator inhibited HIV-1- and CXCL10- induced chemotaxis of PBMC. Activated PBMC were isolated from human blood donors and cultured in PHA and IL-2 for 2 days. Chemotaxis of PBMCs by culture supernatants collected from HIV-1 and CXCL10-treated HFA were done using a modified Boyden chamber. (A) Culture supernatants from HFA after 48 h of treatment with HIV-1 or a combination of HIV and CXCL10 were used in chemotaxis assays. CXCL10 (100 ng/ml) was used as a positive control (first bar). (B) HFA were pretreated with bryostatin (25 nM) for 30 minutes, then treated with a combination of HIV-1 (250 ng/ml p24) and CXCL10 (10 ng/ml) for 48 h. Culture supernatants were used in chemotaxis of PBMC. In parallel, supernatants from HFN cultures treated with a combination of HIV-1 and TNF-α were also used (P < 0.05) (n = 2). PKC, protein kinase C; PBMC, peripheral blood mononuclear cells; HFA, human fetal astrocytes; HFN, human fetal neurons.