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


Grande et al. Journal of Inflammation 2010 7:19   doi:10.1186/1476-9255-7-19

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