Peterson P K, Gekker G, Hu S, Schoolov Y, Balfour H H, Chao C C
Neuroimmunobiology and Host Defense Laboratory, Minneapolis Medical Research Foundation, MN.
J Neuroimmunol. 1992 Nov;41(1):81-7. doi: 10.1016/0165-5728(92)90198-t.
Culture supernatants from lipopolysaccharide (LPS)-treated murine microglial cells were found to markedly induce the expression of human immunodeficiency virus (HIV)-1 in the chronically infected human promonocytic cell line U1 as detected by measurements of HIV-1 p24 antigen release into U1 culture supernatants. Antibody to tumor necrosis factor (TNF)-alpha had an inhibitory effect on the induction of virus by microglial cell supernatants. Also, treatment of microglia with pentoxifylline, an inhibitor of TNF-alpha production, resulted in suppressed amounts of TNF in the supernatants of LPS-treated microglia and in a reduced stimulatory capacity of these supernatants on HIV-1 expression in U1 cells. These findings support the concept that TNF-alpha production by glial cells plays a pathogenetic role in HIV-1-associated brain disease by promoting the expression of the virus in infected cells.
通过测量释放到U1培养上清液中的人类免疫缺陷病毒（HIV）-1 p24抗原，发现脂多糖（LPS）处理的小鼠小胶质细胞的培养上清液可显著诱导慢性感染的人类原单核细胞系U1中HIV-1的表达。肿瘤坏死因子（TNF）-α抗体对小胶质细胞上清液诱导病毒具有抑制作用。此外，用TNF-α产生抑制剂己酮可可碱处理小胶质细胞，导致LPS处理的小胶质细胞上清液中TNF含量降低，且这些上清液对U1细胞中HIV-1表达的刺激能力减弱。这些发现支持了这样一种观点，即神经胶质细胞产生的TNF-α通过促进病毒在感染细胞中的表达，在HIV-1相关脑病中发挥致病作用。
