Figure 5.

Suppression of autophagy in neurons by CXCL12(5-67) and FIV infection. A) CXCL12(5-67) reduced human neuronal viability in terms of β-tubulin immunoreactivity (i) and cell counts/hpf (ii). B) CXCL12(5-67) exposure reduced LC3 immunoreactivity (i) by >50% in human primary neurons (ii). C) LC3 immunoreactivity, including its lipidated form, was detectable in human neuronal (LAN-2) cells, but CXCL12(5-67) exposure reduced LC3 immunoreactivity, which was blocked by concomitant CXCL11(5-73) treatment (i), although CXCL11(5-73) alone did not affect LC3 expression (ii). D) LC3 immunoreactivity (i) was suppressed in the brains of FIV-infected animals but was rescued by ddI treatment (ii). E) The autophagy-associated gene atg5 was suppressed in brains of FIV⁺ animals, although this change was partially reversed by ddI treatment. *P < 0.05; Dunnet multiple comparison test.