Largen P J, Tam F W, Rees A J, Cattell V
Department of Histopathology, St. Mary's Hospital Medical School, London, UK.
Exp Nephrol. 1995 Jan-Feb;3(1):34-9.
In proliferative glomerulonephritis glomeruli are the target of an inflammatory reaction involving macrophage recruitment and activation. We examined the role of mesangial cells in this process. Supernatants from basal, IL-1, IFN-tau or LPS-stimulated rat mesangial cells (MCS) were tested for chemotactic, colony-stimulating and activation effects on macrophages in vitro. IL-1-stimulated MCS produced a macrophage chemoattractant (p = 0.007 compared with basal MCS) and MCP-1 mRNA was detected in IL-1-stimulated mesangial cells. LPS or IL-1-stimulated MCS produced colony-stimulating activity (LPS p < 0.05, IL-1 p < 0.01, compared with basal MCS or control supernatant, CS). Macrophage activation, assessed by nitric oxide generation, was suppressed. This evidence from functional bioassays supports a selective role for mesangial cells in the control of macrophage-induced glomerular injury, whereby activated mesangial cells participate in the recruitment and proliferation of infiltrating macrophages, and suppresses at least one field of macrophage activation, namely nitric oxide generation.
在增殖性肾小球肾炎中,肾小球是涉及巨噬细胞募集和激活的炎症反应的靶标。我们研究了系膜细胞在此过程中的作用。检测了基础状态、白细胞介素-1(IL-1)、干扰素-tau(IFN-tau)或脂多糖(LPS)刺激的大鼠系膜细胞(MCS)的上清液对巨噬细胞的趋化、集落刺激和激活作用。IL-1刺激的MCS产生了一种巨噬细胞趋化因子(与基础MCS相比,p = 0.007),并且在IL-1刺激的系膜细胞中检测到单核细胞趋化蛋白-1(MCP-1)mRNA。LPS或IL-1刺激的MCS产生了集落刺激活性(与基础MCS或对照上清液相比,LPS p < 0.05,IL-1 p < 0.01)。通过一氧化氮生成评估的巨噬细胞激活受到抑制。来自功能生物测定的这些证据支持系膜细胞在控制巨噬细胞诱导的肾小球损伤中具有选择性作用,即活化的系膜细胞参与浸润巨噬细胞的募集和增殖,并抑制巨噬细胞激活的至少一个方面,即一氧化氮生成。