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HIV‐1 Tat Protein Amplifies Amyloid beta‐induced Inflammatory Gene Expression in Brain Endothelial Cells

One of the emerging problems in HIV/AIDS epidemiology is an increase in the older population affected by HIV infection. We hypothesize that amyloid beta and HIV‐1 Tat can cross‐amplify their effects on inflammatory gene expression in an in vitro BBB model. We employed a co‐culture model of human brain microvascular endothelial cells (HBMEC), transfected with different inflammatory gene promoter constructs, and a human astrocyte cell line which produces HIV‐1 Tat. Treatment of HBMEC with amyloid beta (1–40) resulted in a significant increase in E‐selectin, MCP‐1 and IL‐6 promoter activity in the presence of Tat producing astrocytes. The HMG‐CoA reductase inhibitor simvastatin blocked activation of E‐selectin promoter activity induced by amyloid beta in the presence of Tat producing cells. Our data indicate that exposure of HBMEC to Tat and amyloid beta (1–40) can synergistically potentiate inflammatory responses in the brain endothelium. These effects may contribute to the adhesion and transmigration of HIV‐infected monocytes into the brain. In addition, simvastatin may have a beneficial effect in reducing the BBB inflammatory responses in HIV‐1 infected older patients.