Table 1.

Summary effects of different molecules involved in inflammation in the obstructive nephropathy

Agent	Effect
NF-κB	Inflammatory gene expression Macrophage infiltration Renal tubular cell apoptosis
Ang II	NF-κB activation Oxidative stress TGF-β upregulation Macrophage infiltration
TNF-α	Macrophage infiltration Renal tubular cell death
IL-1	ICAM expression Macrophage infiltration Fibroblast activation
MIF	Leukocyte activation Fibroblast proliferation
E,P,L Selectins	Monocytes/macrophage and T cell infiltration Tubular apoptosis
VCAM, ICAM	Interstitial inflammation Leukocyte infiltration
β-integrins	Macrophage infiltration
MCP-1, RANTES, MIP-1α	Macrophage recruitment
CCR1, CCR2	Leukocyte recruitment Interstitial fibrosis
JAMS	Leukocyte recruitment
M-CSF	Macrophage infiltration, activation and proliferation Tubular apoptosis
IP-10	Leukocyte recruitment
TGF-β	Monocyte/macrophage infiltration Fibroblast proliferation Tubular apoptosis
HGF	Suppress macrophage infiltration Inhibit chemokine expression
OPN	Macrophage infiltration Interstitial fibrosis Repress tubular cell apoptosis
iNOS	Resistance to cell death Limit macrophage infiltration