In proliferative glomerulonephritis glomeruli are the target of an inf
lammatory reaction involving macrophage recruitment and activation. We
examined the role of mesangial cells in this process. Supernatants fr
om basal, IL 1, IFN-tau or LPS-stimulated rat mesangial cells (MCS) we
re tested for chemotactic, colony-stimulating and activation effects o
n macrophages in vitro. IL-1-stimulated MCS produced a macrophage chem
oattractant (p = 0.007 compared with basal MCS) and MCP-1 mRNA was det
ected in IL-1-stimulated mesangial cells. LPS or IL-1-stimulated MCS p
roduced colony-stimulating activity (LPS p < 0.05, IL-1 p < 0.01, comp
ared with basal MCS or control supernatant, CS). Macrophage activation
, assessed by nitric oxide generation, was suppressed. This evidence f
rom functional bioassays supports a selective role for mesangial cells
in the control of macrophage-induced glomerular injury, whereby activ
ated mesangial cells participate in the recruitment and proliferation
of infiltrating macrophages, and suppresses at least one field of macr
ophage activation, namely nitric oxide generation.