Tubular cell and HIV-1 gp120 interaction products promote migration of monocytes.

Renal interstitial accumulation of monocytes is an important feature of HIV-associated nephropathy. We studied the effects of proximal tubular cell products (TCP) and proximal tubular cell-gp120 interaction products (TC-120IP) on the migration of monocytes across a modified Boyden chamber. TC-120IP promoted (P < 0.001) the migration of monocytes when compared with TCP (TCP, 45.0 +/- 5.9 vs. TC-120IP, 192.3 +/- 39.5 migrated monocytes/field). This effect of TC-120IP on monocyte migration was dose dependent. Anti-MCP-1 (TCP, 24.7 +/- 2.6; TC-120IP, 82.3 +/- 5.5; TC120-IP + anti-MCP-1 antibody, 46.5 +/- 3.5 migrated monocytes/field) as well as anti-TGF-beta antibodies (TCP, 25.8 +/- 3.4; TC120-IP, 80.3 +/- 6.9; TC-120IP + anti-TGF-beta antibody, 43.8 +/- 5.6 migrated monocytes/field) partly attenuated TC-120IP-induced migration of monocytes across a filter. Moreover, anti-MCP-1 and anti-TGF antibodies showed an additive inhibitory effect on TC-120IP-induced migration of monocytes across a filter. These results suggest that TC-120IP-induced migration of monocytes may be mediated through the generation of MCP-1 and TGF-beta by tubular cells. The present study provides the basis for a hypothesis that HIV-1 gp120 protein may be contributing to the infiltration of monocytes in the renal interstitium of patients with HIV-associated nephropathy.